CN115466742A - Cancer gene VGLL1 and application of coding protein thereof - Google Patents

Cancer gene VGLL1 and application of coding protein thereof Download PDF

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CN115466742A
CN115466742A CN202210609994.1A CN202210609994A CN115466742A CN 115466742 A CN115466742 A CN 115466742A CN 202210609994 A CN202210609994 A CN 202210609994A CN 115466742 A CN115466742 A CN 115466742A
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vgll1
ovarian cancer
cancer
gene
expression
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夏建川
李涵
蔡黎明
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Sun Yat Sen University
Sun Yat Sen University Cancer Center
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Sun Yat Sen University
Sun Yat Sen University Cancer Center
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Abstract

The invention discloses an application of a cancer gene VGLL1 and an encoding protein thereof, and particularly discloses an application of the VGLL1 gene and/or the encoding protein thereof in preparation of a medicament for treating cancer, and an application of the VGLL1 gene and/or the encoding protein thereof in preparation of a reagent or a kit for diagnosis and/or prognosis of cancer. The invention discovers that the oncogene VGLL1 plays an important role in the generation and development processes of tumors, and the high expression of VGLL1 can induce malignant progresses such as invasion and metastasis of ovarian cancer. The research result also shows that the induction of conditional down-regulation of VGLL1 can effectively relieve the growth of ovarian cancer cells and inhibit the invasion and metastasis capacity of the ovarian cancer cells. The invention provides a new diagnosis and treatment idea and a drug screening platform for solving the clinical problems of ovarian cancer metastasis and the like.

Description

Cancer gene VGLL1 and application of coding protein thereof
Technical Field
The invention belongs to the technical field of biology, relates to a novel oncogene and application of a coding protein thereof, and particularly relates to an oncogene VGLL1 and application of a coding protein thereof.
Background
At present, the incidence rate of ovarian cancer is the first of female malignant tumors in the world, and the incidence rate of ovarian cancer is showing a trend of youthfulness, which becomes an important factor threatening the health of women. The treatment modalities for ovarian cancer vary from region to region and from hospital to hospital, and generally include surgery, radiation therapy, systemic therapy, and the like. 70% of patients with ovarian cancer have metastasis during primary diagnosis, cytoreductive surgery and adjuvant chemotherapy have metastasis, and the treatment scheme of cytoreductive surgery and adjuvant chemotherapy is difficult to achieve the curative effect, and more than 70% of patients have relapse. However, the specific mechanism by which ovarian cancer metastasizes is unclear, with the peritoneum being the most common site of ovarian cancer metastasis, and patients with peritoneal metastasis have a 5-year survival rate of less than 30%. Among them, omentum is most vulnerable as an important component of the peritoneum, and tumor progression is accelerated by omental metastasis with ascites formation. It can be seen that the specific mechanism of omentum metastasis of ovarian cancer is determined, and a target for inhibiting ovarian cancer metastasis is found, which is important for improving ovarian cancer treatment.
High mobility group proteins (HMG) are generally classified into three superfamily HMG1/HMG2, HMG14/HMG17 and HMGA 1. The protein of HMGA1 has the function of a structural transcription factor, is involved in the structural activation of target gene initiation factors of various pathways and is related to different cell processes, including the regulation and control of the expression of induced genes; HMGA1 protein replaces H1 histone at the relevant site, thereby altering chromatin structure; inducing a neoplastic transformation; promote the proliferation and migration of tumor cells. Recent studies have shown that HMGA1 is involved in the transcriptional regulation of many tumor-associated genes and binds to nuclear backbone binding sequences (MARs/SARs) that anchor chromatin to the central position of the nucleus and organize independent DNA regions that function both in RNA transcription and translation into topological structures, thereby altering chromatin structure and further activating chromatin transcription. HMGA1 may cause malignant progression of tumors through transcriptional regulation of the above-mentioned tumor-associated genes.
TEAD transcription factor is also called transcription enhancement factor, is a key part of Hippo-YAP signal transmission, and regulates the processes related to cell proliferation, differentiation and the like. In mammals, TEAD has a highly conserved domain, with four component members, TEAD1-4, comprising a TEA domain (DBD) that binds DNA, and a transactivation domain (YBD) that interacts with a transcription coactivator (YAP/TAZ) and expression of multiple genes associated with apoptosis. Among the TEAD family, especially TEAD1 and TEAD4 are significantly associated with the development of various cancers, whose function dominates throughout the family. For example, studies have shown that TEAD1 can modulate the cancer biomarker mesothelin, which is overexpressed in a variety of tumors, and that the synergistic effect of TEAD1 with YAP can induce cell growth and can also up-regulate oncogenes, leading to the exacerbation of cutaneous melanoma and embryonic rhabdomyosarcoma. TEAD4 is also an important transcription factor which has been reported many times in recent years, and promotes cancer cell proliferation and metastasis in various cancers such as gastric cancer and colorectal cancer. And TEAD4 was also shown to independently exert transcriptional regulatory functions independent of YAP/TAZ. Changes in the subcellular localization of TEAD are an important mechanism by which TEAD regulates its transcriptional activity independently of the Hippo signaling pathway. Interestingly, both dependent and independent of YAP/TAZ, increases in TEADs expression and activity are associated with the progression of several solid tumors (e.g., breast, colorectal, pancreatic, prostate), and thus TEADs are also important mediators of tumor progression and therapeutic targets.
VGLL1 (Vestial-like 1) is the Drosophila transcription coactivator Vestial (Vg), a family of which consists primarily of VGLL1-4, which contains the TOUDU domain, mediating interactions with TEA domain transcription factors (TEADs). Researches show that VGLL1 is highly expressed in gastric cancer, breast cancer and ovarian cancer and has the effect of promoting malignant progression of tumors. The research result shows that VGLL1 can be used as a transcription co-activator to be combined with TEAD4, and can be used for transcriptionally activating HMGA1, so that the Wnt/beta-catenin signal path is activated, and malignant progresses such as ovarian cancer cell proliferation, invasion and metastasis are induced. Therefore, more practical theoretical bases are provided for solving the problems of invasion and metastasis of ovarian cancer and the like by exploring the molecular mechanism, and the construction of a VGLL1 expression detection kit and the design of a medicament targeting VGLL1 are particularly important for diagnosis and treatment of ovarian cancer.
Disclosure of Invention
The invention aims to provide a novel oncogene VGLL1 (vascular Like Family Member 1) and application of a protein encoded by the same.
The invention researches the expression characteristics and the regulation mechanism of VGLL1 in tumor tissues, particularly ovarian cancer, researches the new functions of VGLL1 and provides new application of VGLL1.
In order to realize the purpose, the technical scheme is as follows:
the invention provides application of VGLL1 gene and/or encoded protein thereof in preparation of a medicament for treating cancer.
The invention provides an application of a reagent for reducing VGLL1 gene expression and/or a reagent for reducing VGLL1 protein in preparation of a medicine for treating cancer.
Preferably, the agent that reduces expression of the VGLL1 gene comprises an shRNA that reduces expression of the VGLL1 gene; more preferably, the sequence of the shRNA is as set forth in SEQ ID NO:4 and/or SEQ ID NO: 5. as shown.
Preferably, the treatment of cancer comprises inhibiting the growth of tumor cells, inhibiting the metastasis of tumor cells, inhibiting the tumorigenicity of tumor cells, and/or inducing apoptosis of tumor cells.
The invention provides application of VGLL1 gene and/or its coded protein in preparing a reagent or a kit for cancer diagnosis and/or prognosis judgment.
The invention provides application of a reagent for detecting VGLL1 in preparing a reagent or a kit for cancer diagnosis and/or prognosis judgment.
Preferably, the reagent for detecting VGLL1 comprises a sequence shown in SEQ ID NO:1 and SEQ ID NO:2 and/or VGLL1 antibody.
Preferably, the cancer is ovarian cancer.
The invention provides a medicine for treating cancer, which comprises shRNA for reducing VGLL1 gene expression, wherein the sequence of the shRNA is shown as SEQ ID NO:4 and/or SEQ ID NO:5, respectively. Preferably, the cancer is ovarian cancer.
The invention provides a reagent or a kit for cancer diagnosis and/or prognosis judgment, wherein the reagent or the kit comprises a primer pair for detecting VGLL1 and/or a VGLL1 antibody, and the sequence of the primer pair is shown as SEQ ID NO:1 and SEQ ID NO:2. preferably, the cancer is ovarian cancer.
Has the advantages that:
the invention discovers a novel oncogene VGLL1 in ovarian cancer tumor cells, and the VGLL1 is detected and found in a large number of clinical samples to show higher expression level in ovarian cancer patients and is closely related to the poor prognosis of the patients and the generation of endocrine therapy tolerance phenomena. In vivo and in vitro functional research and analysis show that VGLL1 can effectively promote the proliferation of ovarian cancer cells and promote the apoptosis of the ovarian cancer cells. By inhibiting the VGLL1 expression level of ovarian cancer cells, the invasion and metastasis capacity of the ovarian cancer cells is inhibited. In conclusion, the research finds that VGLL1 plays an important role in the malignant development process of ovarian cancer, and VGLL1 can promote malignant proliferation and metastasis of tumor cells, so that the invention provides a new diagnosis and treatment strategy and a new drug screening platform for treating ovarian cancer.
Drawings
FIG. 1 shows the expression of VGLL1 in public database TCGA, and 10 fresh clinical samples (5 primary lesions of ovarian cancer VS 5 tissues of peritoneal metastatic carcinoma) from this center; expression abundance of primary foci of metastasis: expression abundance of metastases. FIG. 2 shows VGLL1 expression in 7 pairs of ovarian cancer patient tissues and normal ovarian tissues, ovarian cancer cell lines.
FIG. 3 shows that the high expression of VGLL1 is closely related to the metastasis and poor prognosis of ovarian cancer patients, and is consistent with the analysis result of the public database KM-plotter.
FIG. 4 shows that stable ovarian cancer cell lines with high VGLL1 expression and low VGLL1 expression are constructed.
FIG. 5 shows that changes in the expression level of VGLL1 affect the proliferative and metastatic capacity of ovarian cancer cells in vitro.
FIG. 6 shows that changes in VGLL1 expression levels affect the ability of ovarian cancer cells to neoplasia in vivo and to form distant metastases; the sequence corresponding to shVGLL1#1 in the figure is sh-1, and shVGLL1#, 1/VGLL1 is that VGLL1 is silenced and then VGLL1 is overexpressed.
Figure 7 shows that in ovarian cancer, a doxycycline (Dox) inducible expression system was constructed in ovarian cancer cells to inducibly down-regulate the expression of VGLL1. Through in vivo animal experiments, we observed that tumor growth and distant metastasis can be significantly inhibited by Dox-induced low expression of VGLL1. Therefore, VGLL1 is considered to be a potential therapeutic target for improving the clinical prognosis of ovarian cancer patients.
The specific implementation method comprises the following steps:
to better illustrate the objects, aspects and advantages of the present invention, the present invention will be further described with reference to specific examples.
The invention is further described with reference to the drawings and the following detailed description, which are not intended to limit the invention in any way. The reagents, methods and apparatus employed in the present invention are conventional in the art, except as otherwise indicated.
Unless otherwise indicated, reagents and materials used in the following examples are commercially available.
RNA-seq high throughput sequencing (results are shown in FIG. 1A-C)
The method comprises the following steps: the RNA of 5 cases of ovarian cancer primary foci and 5 cases of cancer tissues of peritoneal metastases are extracted for high-throughput sequencing, and the VGLL1 is found to be remarkably highly expressed in the cancer tissues of the peritoneal metastases, is verified by Western-blot assistance, and is consistent with the sequencing result.
IHC detection of VGLL1 expression in clinical specimens of ovarian cancer patients (results are shown in FIG. 2A-E)
When the VGLL1 specific antibody is used for detection in ovarian cancer tissues (a primary focus of a metastatic focus VS) and normal ovarian tissue sections, the result shows that VGLL1 is remarkably upregulated in the ovarian cancer tissues relative to the normal ovarian tissues, and more importantly, VGLL1 is remarkably upregulated in the metastatic ovarian cancer tissues relative to the non-metastatic ovarian cancer tissues.
VGLL1 high expression has clinical significance (results are shown in FIG. 3A-D)
Statistical analysis through SPSS shows that the high expression of VGLL1 in clinical samples is closely related to the low survival rate and the low recurrence-free survival rate of ovarian cancer patients.
4. Construction of stable VGLL1 high-expression and low-expression ovarian cancer cell lines (results are shown in A-B in FIG. 4)
Ovarian cancer cell lines A2780 and OVCAR3 were cultured in DMEM medium (DMEM; gibco BRL) supplemented with 10% fetal bovine serum (Gibco BRL) in a carbon dioxide incubator at 37 ℃.
(1) Construction of expression plasmid for VGLL1
The full-length cDNA sequence of VGLL1 is amplified by PCR, and the primer sequences are as follows:
F：GGATGAACACTTCTCCAGAGCTC
R：ATGGAGACGAGTAACGCCACTG
and constructing the purified VGLL1 full-length sequence onto a pLVX-IRES-puro expression vector to obtain a VGLL1 expression plasmid pLVX-VGLL1.
(VGLL 1 full-length sequence:
ATGGAAGAAATGAAGAAGACTGCCATCCGGCTGCCCAAAGGCAAACAGA AGCCTATAAAGACGGAATGGAATTCCCGGTGTGTCCTTTTCACCTACTTCC AAGGGGACATCAGCAGCGTAGTGGATGAACACTTCTCCAGAGCTCTGAG CAATATCAAGAGCCCCCAGGAATTGACCCCCTCGAGTCAGAGTGAAGGT GTGATGCTGAAAAACGATGATAGCATGTCTCCAAATCAGTGGCGTTACTC GTCTCCATGGACAAAGCCACAACCAGAAGTACCTGTCACAAACCGTGCCG CCAACTGCAACTTGCATGTGCCTGGTCCCATGGCTGTGAATCAGTTCTCAC CGTCCCTGGCTAGGAGGGCCTCTGTTCGGCCTGGGGAGCTGTGGCATTTC TCCTCCCTGGCGGGCACCAGCTCCTTAGAGCCTGGCTACTCTCATCCCTTC CCCGCTCGGCACCTGGTTCCAGAGCCCCAGCCTGATGGGAAACGTGAGCC TCTCCTAAGTCTCCTCCAGCAAGACAGATGCCTAGCCCGTCCTCAGGAAT CTGCCGCCAGGGAGAATGGCAACCCTGGCCAGATAGCTGGAAGCACAGG GTTGCTCTTCAACCTGCCTCCCGGCTCAGTTCACTATAAGAAACTATATGT ATCTCGTGGATCTGCCAGTACCAGCCTTCCAAATGAAACTCTTTCAGAGTT AGAGACACCTGGGAAATACTCACTTACACCACCAAACCACTGGGGCCAC CCACATCGATACCTGCAGCATCTTTAG)。
(2) transfection of ovarian cancer cells
The obtained pLVX-VGLL1 and pLVX empty vector (pLVX-vector) as a control were transferred into 293FT cells using Lipofectamine2000 (Invitrogen, # 11668) and optimized packaging plasmid (Invitrogen, K4975-00), respectively, and supplemented with DMEM medium supplemented with 10% fetal bovine serum after 12 hours. Lentivirus supernatants were collected after 48 and 72 hours and infected with a2780 and OVCAR3 cell lines. Stable VGLL1 over-expressed cell strains A2780-VGLL1 and OVCAR3-VGLL1 can be obtained by screening for about 2 weeks with puromycin (2 ug/mL; thermo Fisher, A1113802), and control cell strains are A2780-Vec and OVCAR3-Vec respectively.
5. Construction of ovarian cancer cell strain capable of stably silencing VGLL1 expression
Ovarian cancer cell lines A2780 and OVCAR3 were cultured in DMEM medium (DMEM; gibco BRL) supplemented with 10% fetal bovine serum (Gibco BRL) in a carbon dioxide incubator at 37 ℃. VGLL1-shRNA (sh-1:5 ' -GGTGATGGTCCAGAATTAAGA-3 '; sh-2:5' -GCCAGTACCAGCCTTCCAAAT-3) stably expressing specific interference sequences and a negative control (psiHIV-Ct 1) were provided by GeneCopoeia, inc., VGLL1-shRNA1,2 and psiHIV-Ct1 as a control were transferred into 293FT cells using Lipofectamine2000 (Invitrogen, 11668) and optimized packaging plasmids (GeneCopoeia, HPK-LvTR), and the medium DMEM medium (Gibco BRL) was replaced after 12 hours with 10% fetal bovine serum (Gibco BRL). 24. Retroviral supernatants were collected continuously after hours and transduced into the a2780 and OVCAR3 cell lines. After 48 hours of transfection, stable VGLL 1-silenced cell strains A2780-sh1, A2780-sh2, OVCAR3-sh1 and OVCAR3-sh2 and corresponding control cell strains A2780-Ct1 and OVCAR3-Ct1 are obtained by screening with 3 mu G/mL of G418 (Geneticin) for about 2 weeks.
6. Detection of VGLL1 Gene expression
All the cell strains established above need to be detected on the protein level by Western-blot to detect the expression of VGLL1.
VGLL1 antibody: 10124-2-AP (Proteitech Group, inc, USA)
7. Detection of proliferation potency of ovarian cancer cells (results are shown in FIG. 5)
(1) In vitro experiments: cell growth experiments (results are shown in FIG. 5, A)
The change of the growth rate of the cells with high expression of VGLL1 and silence of VGLL1 is detected by MTT experiment. The experimental procedures were performed according to the instructions of the cell proliferation MTT kit (Roche, mannheim). Briefly described as follows: respectively dividing the experimental group cells and the control group cells into 1 × 10 4 One cell/well was inoculated in a 24-well plate, 100. Mu.L of MTT labeling mixture at l0.3mg/mL was added to one group of cells every 24 hours, and after 4 hours of incubation, absorbance (OD value) was measured with a microplate reader (Tecan), and this experiment was repeated 3 times in parallel.
And (4) analyzing results: MTT experiment results show that high expression of VGLL1 can promote growth of ovarian cancer cells, and silencing VGLL1 inhibits growth of the ovarian cancer cells.
(2) In vitro experiments: plate clone formation assay (results are shown in FIG. 5, B)
The experimental and control cells were seeded in 6-well plates at 1X 10 cells per well, respectively 3 And (4) respectively. After 10 days of routine culture, colonies were counted by staining with crystal violet, and this experiment was repeated 3 times in parallel, and the mean and standard deviation were calculated.
And (4) analyzing results: the experimental results show that VGLL1 promotes the clonogenic capacity of ovarian cancer cells.
(2) In vitro experiments: edU proliferation assay (results C-D in FIG. 5)
The cells of the experimental group and the cells of the control group were inoculated into 96-well plates at 1X 10 per well, respectively 3 And (4) respectively. After adherence, the numbers of EdU + cells were counted by staining with EdU (5-ethynyl-2' deoxyuridine), and this experiment was repeated 3 times in parallel, and the mean and standard deviation were calculated.
(3) In vivo experiments: subcutaneous tumor formation experiment (results are shown in A-C in FIG. 6)
Will be 1 × 10 6 The cells of the experimental group and the cells of the control group (A2780-vector) were injected into the left back of 8 nude mice aged 4 weeks or so, respectively. After 35 days, the tumor growing on the nude mice is removed, and after 25 days, the tumor volume, the tumor and the survival rate of the nude mice are counted.
And (4) analyzing results: the results show that VGLL1 high expression is significantly negatively correlated with survival of mice after tumor resection, and VGLL1 high expression clearly indicates a poor prognosis. Therefore, VGLL1 can be a potential indicator of poor prognosis in ovarian cancer patients.
8. Analysis of transferring ability of ovarian cancer cells in vivo
In vivo experiments: model of tumor metastasis in nude mice (results are D-K in FIG. 6)
(1) 10 nude mice were injected with 1X 10 injections via tail vein 6 Individual experimental and control cells. The formation of metastatic tumor nodules in the lung and the survival of nude mice were examined 3 months after injection. After the animals died, the lungs of each group of animals were collected and stained with picric acid and H&E staining further confirmed the number of tumor clones formed in the lung. (2) Respectively injecting 1 × 10 into 10 nude mice by intraperitoneal injection 6 Individual experimental and control cells. And detecting the conditions of the peritoneum, the mesentery and the nodes transferred on the omentum macrocephalum of the nude mouse after 2 months after injection and the survival condition of the nude mouse. And (4) analyzing results: the high expression of VGLL1 inhibits the tumor formation capability of ovarian cancer cells in lung organs and peritoneum, and indicates that VGLL1 has the effect of inhibiting the metastasis of ovarian cancer cells.
9. Therapeutic effect of targeted VGLL 1:
in the ovarian cancer cell line a2780, OVCAR3, doxycycline (doxycline, dox) inducible expression system was constructed to inducibly down-regulate the expression of VGLL1, and the success of Dox system construction was verified by Western blot (a in fig. 7). Through in vivo animal experiments, we observed that tumor growth and distant metastasis and malignant progression were significantly inhibited by Dox-induced low expression of VGLL1 (B-I in fig. 7). Therefore, VGLL1 is considered to be a potential therapeutic target for improving the clinical prognosis of ovarian cancer patients.
The invention discloses a cancer gene VGLL1 and clinical application of an encoding protein thereof. The inventor conducts in-vivo and in-vitro functional research on the oncogene VGLL1, and research results show that the oncogene VGLL1 plays an important role in the generation and development processes of tumors, and the high expression of VGLL1 can induce malignant progression such as invasion and metastasis of ovarian cancer. To further determine whether VGLL1 can inhibit malignant progression such as invasion, metastasis, etc. of ovarian cancer cells in ovarian cancer, we constructed doxycycline (Dox) inducible expression system in ovarian cancer cells to induce conditional down-regulation of VGLL1 expression. The result shows that the VGLL1 can effectively relieve the growth of the ovarian cancer cells and inhibit the invasion and metastasis of the ovarian cancer cells by inducing conditional down-regulation. The invention provides a new diagnosis and treatment idea and a drug screening platform for solving the clinical problems of ovarian cancer metastasis and the like.
Finally, it should be noted that the above embodiments are only used for illustrating the technical solutions of the present invention and not for limiting the protection scope of the present invention, and although the present invention is described in detail with reference to the preferred embodiments, it should be understood by those skilled in the art that modifications or equivalent substitutions can be made on the technical solutions of the present invention without departing from the spirit and scope of the technical solutions of the present invention.
Sequence listing
<110> Zhongshan university, zhongshan university tumor prevention and treatment center
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<213> Artificial sequence (Artificial)
<400> 1
ggatgaacac ttctccagag ctc 23
<210> 2
<211> 22
<212> DNA
<213> Artificial sequence (Artificial)
<400> 2
atggagacga gtaacgccac tg 22
<210> 3
<211> 777
<212> DNA
<213> Artificial sequence (Artificial)
<400> 3
atggaagaaa tgaagaagac tgccatccgg ctgcccaaag gcaaacagaa gcctataaag 60
acggaatgga attcccggtg tgtccttttc acctacttcc aaggggacat cagcagcgta 120
gtggatgaac acttctccag agctctgagc aatatcaaga gcccccagga attgaccccc 180
tcgagtcaga gtgaaggtgt gatgctgaaa aacgatgata gcatgtctcc aaatcagtgg 240
cgttactcgt ctccatggac aaagccacaa ccagaagtac ctgtcacaaa ccgtgccgcc 300
aactgcaact tgcatgtgcc tggtcccatg gctgtgaatc agttctcacc gtccctggct 360
aggagggcct ctgttcggcc tggggagctg tggcatttct cctccctggc gggcaccagc 420
tccttagagc ctggctactc tcatcccttc cccgctcggc acctggttcc agagccccag 480
cctgatggga aacgtgagcc tctcctaagt ctcctccagc aagacagatg cctagcccgt 540
cctcaggaat ctgccgccag ggagaatggc aaccctggcc agatagctgg aagcacaggg 600
ttgctcttca acctgcctcc cggctcagtt cactataaga aactatatgt atctcgtgga 660
tctgccagta ccagccttcc aaatgaaact ctttcagagt tagagacacc tgggaaatac 720
tcacttacac caccaaacca ctggggccac ccacatcgat acctgcagca tctttag 777
<210> 4
<211> 21
<212> DNA
<213> Artificial sequence (Artificial)
<400> 4
ggtgatggtc cagaattaag a 21
<210> 5
<211> 21
<212> DNA
<213> Artificial sequence (Artificial)
<400> 5
gccagtacca gccttccaaa t 21

Claims (10)

  1. Application of VGLL1 gene and/or its coded protein in preparing medicine for treating cancer.
  2. 2. Use of an agent that reduces the expression of a VGLL1 gene and/or an agent that reduces VGLL1 protein in the preparation of a medicament for the treatment of cancer.
  3. 3. The use of claim 1 or 2, wherein the agent that reduces expression of the VGLL1 gene comprises an shRNA that reduces expression of the VGLL1 gene; preferably, the sequence of the shRNA is as shown in SEQ ID NO:4 and/or SEQ ID NO:5, respectively.
  4. 4. The use of claim 1 or 2, wherein the treatment of cancer comprises inhibiting the growth of tumor cells, inhibiting the metastasis of tumor cells, inhibiting the tumorigenicity of tumor cells, and/or inducing apoptosis of tumor cells.
  5. Application of VGLL1 gene and/or encoding protein thereof in preparing reagent or kit for cancer diagnosis and/or prognosis judgment.
  6. 6. Application of a reagent for detecting VGLL1 in preparation of a reagent or a kit for cancer diagnosis and/or prognosis judgment.
  7. 7. The use of claim 6, wherein the reagent for detecting VGLL1 comprises the sequence set forth in SEQ ID NO:1 and SEQ ID NO:2 and/or VGLL1 antibody.
  8. 8. The use of any one of claims 1-7, wherein the cancer is ovarian cancer.
  9. 9. The medicine for treating cancer is characterized by comprising shRNA for reducing the expression of a VGLL1 gene, wherein the sequence of the shRNA is shown as SEQ ID NO:4 and/or SEQ ID NO:5, respectively.
  10. 10. A reagent or a kit for cancer diagnosis and/or prognosis, which is characterized in that the reagent or the kit comprises a primer pair for detecting VGLL1 and/or a VGLL1 antibody, wherein the sequence of the primer pair is shown as SEQ ID NO:1 and SEQ ID NO:2.
CN202210609994.1A 2022-05-31 2022-05-31 Cancer gene VGLL1 and application of coding protein thereof Pending CN115466742A (en)

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Application Number Priority Date Filing Date Title
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Publications (1)

Publication Number Publication Date
CN115466742A true CN115466742A (en) 2022-12-13

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Country Status (1)

Country Link
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