CN110151976B - Application of ZNF496 protein in improving sensitivity of cervical cancer chemotherapy drugs - Google Patents
Application of ZNF496 protein in improving sensitivity of cervical cancer chemotherapy drugs Download PDFInfo
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Abstract
The invention discloses application of ZNF496 protein in improving drug sensitivity of cervical cancer chemotherapy. The ZNF496 overexpression vector is used for stably transfecting and/or transiently transfecting cervical cancer cell strains respectively, and chemotherapy medicament cisplatin treatment is applied, so that the induction of cisplatin on cervical cancer cell apoptosis is increased; the inhibition effect of cisplatin on the cervical cancer cell proliferation is increased through the stable overexpression of ZNF 496; ZNF496 can effectively enhance the inhibition effect of cisplatin on the growth of cervical cancer cells in vivo. The invention has the advantages that: provides a new target and a treatment strategy for solving the problem of increasing the sensitivity of cervical cancer chemotherapeutic drugs, can design a specific targeted treatment scheme, is applied to the preparation of ZNF496 overexpression preparation drugs, is combined with chemotherapeutic drugs, carries out accurate individual treatment on cervical cancer patients, and has important application prospect in clinical treatment.
Description
Technical Field
The invention relates to a protein for improving the sensitivity of a cervical cancer chemotherapy medicament, in particular to an application of ZNF496 protein in improving the sensitivity of a cervical cancer chemotherapy medicament, belonging to the field of medicines.
Background
Cervical cancer (Cervical cancer) is the second most common cancer in women and the third leading cause of cancer death in women worldwide, with about 50 million cases of onset and 25 million cases of death each year. The incidence of cervical cancer is rising year by year, the average annual growth rate is 0.6%, and the high incidence age of morbidity and mortality is in an obvious youthful trend. The occurrence of cervical cancer is closely related to the infection of microorganisms including bacteria, viruses and the like, the persistent infection of high-risk HPV is the main risk factor of cervical cancer, and more than 90 percent of cervical cancer is accompanied by the infection of high-risk HPV. However, the final development of cervical cancer after HPV infection is the result of the combined action of multiple stages, multiple pathways and multiple molecular factors. The traditional treatment mode of cervical cancer is surgery plus radiotherapy, and chemotherapy is only used for palliative treatment of patients with advanced stage and recurrence and pelvic external metastasis who cannot be subjected to surgery or radiotherapy. Therefore, the screening and identification of abnormal molecular events at each stage of cervical cancer occurrence and development, the deep understanding of the signal regulation and control mechanism of cervical cancer occurrence and development, the establishment of early diagnosis early warning system, the research and development of novel tumor targeting drugs, and the strategic significance for improving the survival rate of patients with cervical cancer and improving the survival quality of patients are achieved.
Cisplatin (cissplatin) can inhibit the DNA replication process of cancer cells, damage the cell membrane structure of the cancer cells, has a strong broad-spectrum anticancer effect, and is a first-line medicament for treating various solid tumors such as cervical cancer and the like. However, with the progress of tumor treatment, the treatment effect of cisplatin is gradually reduced, some cervical cancer patients are not sensitive to the effect of cisplatin, and chemotherapy resistance can even be generated, so that the clinical application of cisplatin is greatly restricted. The search and discovery of novel antitumor drugs for improving the sensitivity of cisplatin is one of the key problems to be solved urgently in the clinical treatment of cervical cancer.
ZNF496 gene is located on chromosome 1q44, its mRNA total length is 2453 bp, CDS region is 1764 bp, and it can code 587 amino acids. ZNF496 has homologous genes between a variety of species including mice, cattle, chimpanzees, and humans. The ZNF496 protein domain is sequentially provided with SCAN, KRAB, C2HR and 4 serially-repeated zinc fingers from N end to C end. Like other KRAB-type zinc finger proteins, the SCAN and KRAB domains of ZNF496 primarily mediate protein-protein interactions. In addition, C2HR can bind to methyltransferase NSD1 (nuclear receptor binding SET domain protein 1) of H3K36 and exhibit a KAP-1-independent transcription repression function. Nielsen et al first reported that ZNF496 interacts with NSD1 through the C2HR domain, and NSD1 is a histone lysine methyltransferase, and is closely related to Sotos syndrome, childhood acute myeloid leukemia and megatheria. In addition, ZNF496 also interacted with Jarid2 (AT rich interactive domain 2, jumonji), ZNF496 could inhibit the transcription repression function of Jarid2, and Jarid2 plays an important role in embryo development. To date, little has been done on the biological functions and mechanisms of ZNF 496.
Disclosure of Invention
The invention aims to provide the application of the ZNF496 protein in improving the sensitivity of a cervical cancer chemotherapy medicament, the chemotherapy sensitivity of cisplatin to the cervical cancer is enhanced through the expression of the ZNF496 protein, and a new medicament target selection is provided for effectively improving the clinical curative effect of the cervical cancer.
The technical scheme of the invention is as follows:
the application of the ZNF496 protein in improving the sensitivity of the cervical cancer chemotherapeutic drugs provides a new target and a new treatment strategy for solving the problem of improving the sensitivity of the cervical cancer chemotherapeutic drugs.
The ZNF496 overexpression vector is used for respectively stably transfecting and/or transiently transfecting the cervical cancer cell Hela, and the chemotherapy drug cis-platinum is used for treatment, so that the induction of the cis-platinum on the apoptosis of the cervical cancer cell is increased; the inhibition effect of cisplatin on the proliferation of cervical cancer cells is increased through the stable overexpression of ZNF 496; ZNF496 can effectively enhance the inhibition effect of cisplatin on the growth of cervical cancer cells in vivo.
The beneficial effects of the invention are as follows: provides a new factor influencing the sensitivity of the cervical cancer cells to the cisplatin, and lays an experimental foundation for researching the action mechanism of ZNF496 influencing the sensitivity of tumor cell chemotherapy drugs. By utilizing the mechanism, a specific targeted treatment scheme can be designed, and the method is applied to the preparation of ZNF496 overexpression preparation medicines and the combined application of chemotherapeutic medicines, can implement accurate individualized treatment on cervical cancer patients, and has important application prospects in clinical treatment.
The invention is further illustrated by the following figures and examples.
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FIG. 1 shows that Western blot identifies the expression levels of ZNF496 proteins in cervical cancer Hela cells, which are screened after stable transfection of lentiviral overexpression vectors and corresponding no-load control vectors, in cervical cancer cell strains pLV-Neo-ZNF496-1, pLV-Neo-ZNF496-2 and no-load control stable cell strains Con;
FIG. 2 shows the effect of stable over-expression of ZNF496 on cisplatin-induced apoptosis of cervical cancer cells in apoptosis experiments (FIG. 2-A shows the apoptosis rate of ZNF496 stable over-expression cervical cancer cell strains pLV-Neo-ZNF496-1, pLV-Neo-ZNF496-2 and an unloaded control stable cell strain Con which are detected by a flow cytometer and are treated by 10 mu M of cisplatin for 24 h; FIG. 2-B shows the statistical comparison of the apoptosis rate among groups; the data comparison between the two groups adopts t test; and represents that the experimental group and the control group have significant difference (P represents 0.05; P represents 0.01));
FIG. 3 shows that Western blot identifies the expression level of ZNF496 protein after transient transfection in cervical cancer Hela cells;
FIG. 4 shows the effect of transient overexpression of ZNF496 on cisplatin-induced apoptosis in cervical cancer cells in apoptosis assay (FIG. 4-A shows the apoptosis rate induced by 10 μ M cisplatin treatment after 18 h transient overexpression of PCMV-Myc-ZNF496 and the corresponding empty-load control plasmid Con in cervical cancer Hela cells by flow cytometry; FIG. 4-B shows the statistical comparison of apoptosis rates between groups; t test is used for the comparison of data between two groups; representing significant difference between the experimental group and the control group (P < 0.05;. P < 0.01;. P < 0.001));
FIG. 5 is a graph showing the effect of stable overexpression of ZNF496 on the proliferation of cisplatin-affected cervical cancer cells (FIG. 5-A shows the cell proliferation after the stable overexpression of ZNF496 in the plate clone formation experiment for 2 weeks after the treatment of 1. mu.M and 1.5. mu.M cis-platin in the plate clone formation experiment for the stable overexpression of ZNF496 in the cervical cancer cell line pLV-Neo-ZNF496-1 and the unloaded control stable cell line Con; FIG. 5-B shows the statistical comparison of the number of cell clones between each group; t test was used for the comparison of data between the two groups;. indicates that the significant difference between the experimental group and the control group (P < 0.05;. P < 0.01;. P < 0.001));
FIG. 6 shows the effect of stable over-expression of ZNF496 on the growth of cisplatin-affected cervical cancer cells in vivo in nude mice subcutaneous tumorigenicity experiments (FIG. 6-A shows that ZNF496 stably over-expressed cervical cancer cell line pLV-Neo-ZNF496-1 and unloaded control stable cell line Con are inoculated into nude mice subcutaneous tissue and treated with cisplatin (1 mg/kg) for 30 days, FIG. 6-B shows the tumor volume growth curve among groups, FIG. 6-C shows the comparison of tumor weight among groups, and t test is used for the comparison of data among two groups). The significant difference between the experimental group and the control group (P < 0.05; P <0.01) is represented.
Detailed Description
The following description of the preferred embodiments of the present invention is provided for the purpose of illustration and description, and is in no way intended to limit the invention.
Example 1
Construction of ZNF496 stable overexpression cervical cancer cell strain
(1) Cloning the CDS full length of the human ZNF496 gene by a molecular biological method;
(2) PCR amplifying and recovering clone products;
(3) connecting the recovered product to a vector pLV-Neo, carrying out double enzyme digestion identification, and sequencing;
(4) the plasmid with correct sequencing and successful construction is subjected to lentivirus packaging:
a.293T cells to 25 cm 2 Two bottles of culture bottles are used for transfection when the cells grow to 80%;
b. two clean 1.5 mL centrifuge tubes were taken in a cell clean bench and 1 mL of antibiotic-free and serum-free medium was added to each tube. One of the tubes was added with the desired plasmid pLV-Neo-ZNF496 (5. mu.g), packaged plasmid psPAX2 (3.75. mu.g), pMD2.G (1.25. mu.g), and mixed well. Adding the target plasmid pLV-Neo (5 mu g) and the packaging plasmid psPAX2 (3.75 mu g) and pMD2.G (1.25 mu g) into the other centrifuge tube, and uniformly mixing;
c. adding 20 mu L of Tracasefect Reagent into each of the two centrifuge tubes, fully mixing, incubating at room temperature for 20 min, and adding into two culture bottles inoculated with 293T cells;
d. supplementing the liquid after 6 h of transfection, changing the liquid of the cells after 22 h, continuously culturing for 50 h, and collecting culture supernatant; filtering at 1200 rpm for 3 min with 0.22 μm filter, and packaging into EP tube;
(5) infecting the packed virus with HeLa cells of human cervical carcinoma for 96 h, and screening by changing the infection time to a culture medium containing G418 medicine until the cells stably survive;
(6) digesting the screened stable cells into single cells, infinitely diluting the single cells into a six-hole plate for continuous culture, picking out the single cell mass when the single cells grow into a single cell mass, and putting the single cell mass into a 24-hole plate containing a fresh culture medium for culture;
(7) and continuously culturing a part of cells, and carrying out Western blot on a part of extracted proteins to identify the expression quantity of ZNF496, thereby screening a HeLa cell strain with ZNF496 stably overexpressed.
The stable overexpression efficiency of ZNF496 was identified by Western blot according to the method of example 1, and the results are shown in FIG. 1. The expression of the ZNF496 protein in stable over-expression cervical cancer cell strains pLV-Neo-ZNF496-1 and pLV-Neo-ZNF496-2 is obviously increased compared with that of an unloaded control stable cell strain Con. The method provides an important tool for further research on drug sensitivity of cervical cancer.
Example 2
Apoptosis experiment for detecting influence of ZNF496 on cisplatin drug sensitivity of cervical cancer cells
(1) ZNF496 over-expressing stable HeLa cell strain, treating with cisplatin, and performing apoptosis experiment
a. Digesting the ZNF496 over-expression stable HeLa cell strains pLV-Neo-ZNF496-1, pLV-Neo-ZNF496-2 and the cells of the no-load control stable strains thereof at 800 rpm for 3 min, and counting;
b. inoculating the same number of ZNF496 over-expression stable HeLa cell strains and no-load control stable strain cells into a six-hole plate;
c. adding medicine when the cells grow to 70% -80%, adding 2 mL of culture medium containing cis-platinum Cisplatin (10 mu M) into each hole of an experimental group, adding 2 mL of culture medium containing the same amount of DMSO into a control group, and collecting the cells after 24 h;
d. the medium in the six-well plate was directly poured off, and after cells were washed once with 1 × PBS, they were digested. The cells were transferred to a 1.5 mL centrifuge tube at 70 Xg for 3 min at 4 ℃;
e. removing supernatant, adding 500 μ L of 1 × PBS, slightly blowing for 3 times (ensuring the same blowing frequency of each sample), 70 × g, 3 min, 4 ℃;
f. removing supernatant, adding 1 × Binding Buffer prepared by 300 μ L of 1 × PBS into each sample, adding 5 μ L of Annexin V/APC and 5 μ L of PI for marking, dyeing for 15 min at normal temperature in a dark place, and slightly blowing cells at intervals of 5 min to fully dye;
g. filtering, placing on ice, and detecting apoptosis change by flow cytometry.
Apoptosis before and after cisplatin treatment of the cervical cancer cell strain and the unloaded control cell strain which are stably overexpressed by the ZNF496 protein are detected by a flow cytometer according to the method of example 2 (1). The results are shown in FIG. 2, the chemotherapy drug cisplatin can induce the apoptosis of the cervical cancer cells, and after the ZNF496 protein is stably over-expressed, the apoptosis rate of cisplatin-induced cells of the pLV-Neo-ZNF496-1 and the pLV-Neo-ZNF496-2 groups is obviously higher than that of Con of the control group. This indicates that ZNF496 stable overexpression can increase the apoptosis rate of cervical cancer cells induced by chemotherapeutic drug cisplatin.
(2) ZNF496 overexpression plasmid transiently transfects HeLa cells, and cisplatin treatment is carried out to carry out apoptosis experiment
The HeLa cells are passaged, 4 holes of a six-hole plate are inoculated, transfection is carried out when the cells grow to 70%, two holes are transfected with ZNF496 over-expression plasmids PCMV-Myc-ZNF496, and two holes are transfected with no-load control plasmids PCMV-Myc with the weight of 2 mu g each; performing Western blot on harvested cells after transient transfection for 18 h, and identifying the expression quantity of ZNF 496;
b. in the drug sensitivity experiment, after plasmid transfection for 18 h, 2 mL of culture medium containing Cisplatin Cisplatin (10 mu M) is replaced for two experimental groups, and 2 mL of culture medium containing the same amount of DMSO is replaced for a control group for treatment;
after c.36 h, the medium in the six well plates was directly poured off, and the cells were washed once with 1 × PBS and digested. The cells were transferred to a 1.5 mL centrifuge tube at 70 Xg for 3 min at 4 ℃;
d. removing supernatant, adding 500 μ L of 1 × PBS, slightly blowing for 3 times (ensuring the same blowing frequency of each sample), 70 × g, 3 min, 4 ℃;
e. removing supernatant, adding 1 × Binding Buffer prepared by 300 μ L of 1 × PBS into each sample, adding 5 μ L of Annexin V/APC and 5 μ L of PI for marking, dyeing for 15 min at normal temperature in a dark place, and slightly blowing cells at intervals of 5 min to fully dye;
f. filtering, placing on ice, and detecting apoptosis change by flow cytometry.
According to the method of example 2 (2) a, the overexpression efficiency of the ZNF496 transient transfection cervical cancer cell is firstly identified by Western blot, and the result is shown in figure 3, compared with the transfected no-load control plasmid, the ZNF496 protein expression in the cervical cancer cell is obviously improved after the ZNF496 transient transfection of the plasmid is transiently transfected. Then, cell apoptosis before and after cis-platinum treatment of the ZNF496 protein transient overexpression cervical cancer cell strain and the no-load control cell strain is detected by a flow cytometer according to the method of example 2 (2) bcdef. The results are shown in FIG. 4, ZNF496 transient overexpression can induce the apoptosis of cervical carcinoma cells, and the apoptosis rate of the ZNF496 transient overexpression cells is obviously increased compared with the apoptosis induction rate of unloaded control cells after the cells are treated by cisplatin. The result further proves that the ZNF496 protein can increase the sensitivity of the cervical cancer cells to the apoptosis induced by the chemotherapeutic drug cisplatin.
Example 3
Plate clone formation experiment for detecting influence of ZNF496 on cisplatin drug sensitivity of cervical carcinoma cells
(1) The same number (1X 10) 3 ) The stable overexpression HeLa cell strain pLV-Neo-ZNF496-1 and the no-load control cell strain of the ZNF496 are inoculated to a six-well plate; every three holes are a plurality of holes;
(2) the experimental group was treated with fresh medium containing Cisplatin cissplatin (1. mu.M, 1.5. mu.M) and the control group with fresh medium containing the same amount of DMSO every three days;
(3) after 2 weeks, observing that if the cell clone number can be counted and is not too much, collecting the plate;
(4) directly pouring out the culture medium, and completely sucking residual liquid by using a liquid moving device; carefully adding 1 mL of methanol solution containing 0.1% crystal violet along the edge of a six-hole plate, and dyeing for 20 min;
(5) carefully pour off the staining solution, slowly wash the six-well plate with tap water, pay attention to not wash out the clones;
(6) after drying in the sun, the photographs were taken for statistical analysis.
The effect of ZNF496 stable overexpression on cisplatin-responsive cervical cancer cell proliferation was examined by plate colony formation assay according to the procedure of example 3 and the results are shown in FIG. 5. The stable over-expression of ZNF496 can inhibit the clone formation of cervical cancer cells; cisplatin treatment with different concentrations can inhibit the clonogenic effect of cervical carcinoma cells, and after over-expression of the ZNF496, the clonogenic number is obviously reduced compared with that of a control group Con, which shows that stable over-expression of the ZNF496 increases the proliferation inhibition effect of cisplatin on the cervical carcinoma cells.
Example 4
In vivo study of ZNF496 affecting susceptibility of cervical cancer to cisplatin drugs
(1) Female nude mice of 4-5 weeks of age were selected, 5 mice per group, at 2X 10 6 In number of individuals, respectively inoculated with ZNF496 overexpression stabilizationCervical cancer cell strain pLV-Neo-ZNF496-1 and no-load control cell strain;
(2) the Cisplatin experimental group is administrated with Cisplatin Cisplatin (1 mg/kg) every two days after inoculation; PBS was administered to the control group;
(3) measuring the long diameter and the short diameter of the tumor by using a vernier caliper every three days, and measuring the weight of the nude mouse by using a balance;
(4) after 30 days of inoculation, the nude mice were sacrificed by cervical dislocation and tumor bodies were detached. Measuring the length, width and height of the tumor and the weight of the tumor;
(5) and (5) drawing a tumor growth curve in the nude mouse.
The effect of ZNF496 stable overexpression on the in vivo growth of cisplatin-affected cervical cancer cells was examined by nude mouse subcutaneous neoplasia experiments in accordance with the procedure of example 4 and the results are shown in FIG. 6. ZNF496 stable overexpression can inhibit the in vivo tumorigenicity ability and tumor size of cervical carcinoma cells; after cisplatin treatment, the tumor forming capability and the tumor size of the cervical cancer cells in a nude mouse are inhibited, and after ZNF496 is over-expressed, the tumor forming capability of the cervical cancer cells in the nude mouse is obviously reduced and the tumor size is also obviously reduced compared with a control group Con. This shows that ZNF496 overexpression obviously improves the inhibition effect of cisplatin on the growth of cervical cancer cells in vivo, and increases the sensitivity of the cervical cancer cells to chemotherapeutic drugs cisplatin.
Claims (6)
1. An application of a preparation for over-expressing ZNF496 protein in preparing a medicament for improving the sensitivity of cervical cancer to a chemotherapeutic medicament cisplatin.
2. Use according to claim 1, characterized in that: respectively stably transfecting and/or transiently transfecting cervical cancer cell strains by using ZNF496 overexpression vectors, and increasing the induction of cisplatin on cervical cancer cell apoptosis by applying chemotherapeutic cisplatin treatment; the inhibition effect of cisplatin on the proliferation of cervical cancer cells is increased by the stable overexpression of ZNF 496.
3. Use according to claim 1, characterized in that: the induction effect of the chemotherapeutic drug cisplatin on the apoptosis of the Hela of the cervical cancer cells is increased through the stable overexpression of ZNF 496.
4. Use according to claim 1, characterized in that: the apoptosis of the cervical cancer cell is induced by ZNF496 transient overexpression, and the induction effect of the chemotherapy medicament cisplatin on the apoptosis of the cervical cancer cell is increased.
5. Use according to claim 1, characterized in that: the in vivo tumorigenesis capacity and tumor size of the cervical cancer cells are inhibited through the stable overexpression of ZNF 496.
6. Use according to claim 1, characterized in that: the tumor forming capability and the tumor size of the cervical cancer cells in vivo are inhibited through cisplatin treatment, and the inhibition effect is more obvious after ZNF496 is over-expressed.
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Citations (2)
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| CN101375860A (en) * | 2008-09-18 | 2009-03-04 | 武汉大学 | Application of cisplatin combined with hTERT-HRP/IAA in medicament for treating cervical cancer cell |
| CN107540736A (en) * | 2016-06-23 | 2018-01-05 | 首都医科大学 | To cervical carcinoma along the related large biological molecule NHERF1 of the property of medicine and its application |
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