CN117165690A - Application of CEP89 as neuroblastoma drug target - Google Patents
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- CN117165690A CN117165690A CN202311411848.9A CN202311411848A CN117165690A CN 117165690 A CN117165690 A CN 117165690A CN 202311411848 A CN202311411848 A CN 202311411848A CN 117165690 A CN117165690 A CN 117165690A
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Abstract
The invention provides an application of CEP89 as a neuroblastoma drug target, and belongs to the technical field of biological medicine. The application provided by the invention comprises the aspects of prognosis, treatment and the like of the neuroblastoma, and solves the problem of lack of a neuroblastoma molecular marker in the prior art. The invention proves that the survival time of the child suffering from the neuroblastoma with high CEP89 expression is short, and shows that CEP89 can be used as a prognosis molecule of the neuroblastoma. In addition, in the human neuroblastoma cell line SK-N-BE2, CEP89 is knocked down to inhibit cell proliferation and migration, which indicates that CEP89 can promote neuroblastoma proliferation and migration, and CEP89 can BE used as a potential treatment target of neuroblastoma.
Description
Technical Field
The invention relates to the technical field of biological medicines, in particular to application of CEP89 as a neuroblastoma drug target.
Background
Neuroblastoma (NB) is the most common malignant extracranial solid tumor in children, with about 90% of cases occurring under 5 years of age, with an average definite age of 2 years, accounting for about 10% of childhood cancer deaths. Neuroblastoma is a cancer of the sympathetic nervous system, particularly sympathetic adrenal progenitor, originating from neural crest cells. NB has significant heterogeneity, exhibits unique and varied biological and clinical characteristics, and although 5-year survival rates of medium and low risk NB patients approach 90%, about 60% of NB patients are high risk, and five-year survival rates are still below 50% despite the adoption of multiple treatment modalities of surgery, chemotherapy, radiation therapy, and biological therapy.
A variety of prognostic parameters have been used for NB tumor classification and risk classification. At present, the clinical NB infant who does not have MYCN gene amplification, ALK gene is normal, DNA ploidy and chromosome 11q are normal, and the clinical NB infant also has the phenomena of low tumor differentiation degree, rapid disease progress, short survival period and the like. Therefore, there is still an urgent need to find new NB molecular markers, which provides basis for clinically developing accurate NB diagnosis and treatment.
Chinese patent CN116359502a discloses the use of ACSS2 as a new target for the treatment of neuroblastoma.
Disclosure of Invention
The invention aims to provide an application of CEP89 as a neuroblastoma drug target, which can be used as a neuroblastoma prognosis molecule and a potential treatment target, and provides a new way for neuroblastoma drug development.
In order to achieve the above object, the present invention provides the following technical solutions:
the present invention provides the use of a prognostic marker comprising CEP89 in the manufacture of a product for assessing the prognosis of neuroblastoma.
The invention also provides a kit for assessing a prognosis of neuroblastoma, the kit comprising reagents for detecting the expression level of CEP89.
Preferably, the reagents for detecting the level of CEP89 expression are primers and/or probes that specifically bind to CEP89.
The invention also provides application of CEP89 as a target in developing or screening or preparing medicaments for preventing and/or treating neuroblastoma.
The invention also provides application of CEP89 as a target in preparing a drug screening model for preventing and/or treating neuroblastoma.
Preferably, the agent is capable of inhibiting the expression of CEP89.
Preferably, the agent comprises interfering RNA, a gene knockout agent or a chemical inhibitor.
The present invention also provides a pharmaceutical composition for preventing and/or treating neuroblastoma, which is capable of inhibiting the expression of CEP89.
Preferably, the pharmaceutical composition comprises a small interfering RNA that is targeted to inhibit CEP89.
The invention also provides a small interfering RNA for targeted inhibition of CEP89, wherein the nucleotide sequence of the small interfering RNA is shown as SEQ ID NO. 1;
and/or the nucleotide sequence of the small interfering RNA is shown as SEQ ID NO. 2.
The invention has the beneficial effects that:
the invention provides a series of applications of CEP89 as a neuroblastoma drug target, including the aspects of prognosis, treatment and the like of the neuroblastoma. The invention proves that the survival time of the child suffering from the neuroblastoma with high CEP89 expression is short, and shows that CEP89 can be used as a prognosis molecule of the neuroblastoma. In addition, in the human neuroblastoma cell line SK-N-BE2, CEP89 is knocked down to inhibit cell proliferation and migration, which indicates that CEP89 can promote neuroblastoma proliferation and migration, and CEP89 can BE used as a potential treatment target of neuroblastoma.
Drawings
Fig. 1 is a graph showing the results of survival curve analysis of CEP89 expression in NB tumors, where a, b: database GSE49711 (SEQC-498) analyzes survival curves. c, d: database GSE16476 (Versteeg-88) analyzes survival curves. Long-rank (Mantel-Cox) test;
FIG. 2 is a graph showing the effect of quantitative PCR detection of CEP89 gene knockdown in SK-N-BE2 cells;
FIG. 3 is a diagram showing the effect of Western blotting in detecting the knockdown of CEP89 gene in SK-N-BE2 cells;
FIG. 4 is a diagram showing the proliferation of SK-N-BE2 cells after the CEP89 gene has been knocked down by comparison, wherein: undyed; the following steps: and (5) crystal violet staining. Scale bar, 500 μm;
FIG. 5 is a graph showing results of RTCA monitoring cell proliferation potency, where NC: negative control, all data statistics using T-test;
FIG. 6 is a graph showing the migration results of neuroblastoma SK-N-BE2 inhibition by CEP89 knockdown, wherein a: cell scratch experiment compares SK-N-BE2 cell migration efficiency after CEP89 gene is knocked down, and scale bar: 500 μm; b: cell mobility of the cell scratch experimental group and the control group is quantitatively counted, and NC: negative control, independent experiments were performed three times, and data statistics were performed using T-test.
Detailed Description
The technical solutions provided by the present invention are described in detail below with reference to examples, but they should not be construed as limiting the scope of the present invention.
Example 1
This example provides the gene CEP89, gene ID:84902.
the statistical analysis of CEP89 expression levels and survival curves in neuroblastoma samples was performed using public databases GSE49711 (SEQC-498) and GSE16476 (Versteeg-88), and the results are shown in FIG. 1.
FIG. 1 shows that the survival rate of the neuroblastoma patients with high CEP89 expression was lower, indicating that the neuroblastoma patients with high CEP89 expression had poor prognosis.
Example 2
This example provides siRNAs knockdown of CEP89 gene (siCEP 89-1# and siCEP 89-2#):
SiCEP89-1#: the nucleotide sequence is GACTGTCCATCGTTTGAAT and is shown as SEQ ID NO. 1;
SiCEP89-2#: the nucleotide sequence is CGTCAAAGATATACAGAAA, shown in SEQ ID NO.2, and is synthesized by RIBOBIO company.
The experimental method is as follows:
human neuroblastoma SK-N-BE2 is cultured in DMEM complete medium containing 10% fetal bovine serum and 1% double penicillin-streptomycin double antibody mixed solution, and placed at 37 ℃ and 5% CO 2 Is cultured in a constant temperature incubator. Cells in the logarithmic growth phase were selected for the experiment. The cell growth state was observed by a microscope.
siRNA transfecting SK-N-BE (2) cells:
negative control siRNA (siCtrl) was purchased from Invitrogen company. SK-N-BE2 cells were trypsinized into individual cells and counted at 1X 10 per well 5 Cell density of each/mL was inoculated into 6-well plates, and after cell density reached about 30%, siRNA (60 nM) was transfected with RNAi MAX (150X) reagent to set an experimental group and a negative control group. After 48h of transfection, the culture medium was changed and a bright field photograph was taken for 72 h. Crystal violet staining: cells were fixed with 4% paraformaldehyde for 15min, stained with crystal violet for 15min, washed several times with pbs, air dried and photographed.
RNA extraction and RT-qPCR analysis:
total RNA from cells was extracted with TRIzol reagent (Invitrogen, cat# 15596018) and cDNA was synthesized with PrimeScript RT Master Mix reverse transcription kit (TakaRa, cat#RR036A). Real-time fluorescent quantitative PCR amplification detection was performed according to the SYBR Green PCR Master Mix kit (BIO-RAD). The reaction condition is 95 ℃ for 15s, 60 ℃ for 1min, 40 loops; the Ct (Cycle threshold) value was read and the relative quantification of CEP89 was referenced to GAPDH.
Western blotting:
cells were quantitated by Western blotting following lysis by NP-40 cell lysis buffer (BOSTER, cat#AR0107). Antibody CEP89 (proteontech, cat# 24002-1-AP), control GAPDH (Cell Signaling Technology, cat# 5174S). Development was performed in a dark room using ECL chemiluminescent kit.
RTCA monitors cell proliferation levels
The cellular activity was monitored in real time using the xcelligent RTCA system without markers. After 24 hours of SK-N-BE (2) transfection, the cells were inoculated in the xCELLigence system, 4X 10 per well 4 And (3) cells. Cell index (cell index) was monitored and recorded by RTCA.
The results of the detection of the knockdown effect at the RNA level after the siRNA (siCEP 89-1# and siCEP 89-1#) are transfected into SK-N-BE2 cells to knock down the CEP89 gene, 72h are shown in FIG. 2, and the knockdown effect is good.
The results of the detection of the knockdown effect at the protein level after the siRNA (sCEP 89-1# and sCEP 89-1#) are transfected into SK-N-BE2 cells to knock down the CEP89 gene, 72h are shown in FIG. 3, and the results show that the knockdown effect is good.
The proliferation of SK-N-BE2 cells after CEP89 gene deletion is observed and compared, the proliferation capacity of the cells is monitored in real time, dynamically and quantitatively by adopting a real-time label-free dynamic cell analysis technology (RTCA), the results are shown in figures 4-5, and the result shows that the SK-N-BE2 cell proliferation can BE inhibited by CEP89 gene deletion.
Cell scratch experiments were further performed:
SK-N-BE2 cells were digested into single cells, counted at 3X 10 5 Cell density per ml was seeded in 6-well plates and after cell attachment, siRNA transient transfection was performed. Transfecting for 24h, wherein the cell confluency is more than 90%, scribing a straight line with a 10 mu L pipette tip perpendicular to the bottom of a 6-well plate, discarding the culture medium, washing the cells 3 times with PBS, removing the scribed cells, adding 2ml DMEM with 2% low serum into each well for culture based on 37 ℃ and 5% CO 2 Is cultured in a constant temperature incubator. The time after the scratch is 0h, the microscope is used for photographing at 0h, 24h and 48h, the scratch width is measured by image J software, the cell migration capacity is expressed by the scratch healing rate, and the scratch is healedThe combination ratio= (0 h scratch width-N h scratch width)/0 h scratch width 100%.
The results are shown in FIG. 6: after the CEP89 gene is knocked down, the cell mobility is obviously reduced, which indicates that the CEP89 gene can be used as an action target for inhibiting the migration of neuroblastoma cells.
The foregoing is merely a preferred embodiment of the present invention and it should be noted that modifications and adaptations to those skilled in the art may be made without departing from the principles of the present invention, which are intended to be comprehended within the scope of the present invention.
Claims (10)
1. Use of a prognostic marker in the manufacture of a product for assessing prognosis of neuroblastoma, wherein said prognostic marker comprises CEP89.
2. A kit for assessing a prognosis of a neuroblastoma, said kit comprising reagents for detecting the expression level of CEP89.
3. The kit of claim 2, wherein the reagents for detecting the expression level of CEP89 are primers and/or probes which bind specifically to CEP89.
Use of cep89 as a target in the development or screening or in the manufacture of a medicament for the prevention and/or treatment of neuroblastoma.
Use of cep89 as a target in the preparation of a drug screening model for the prevention and/or treatment of neuroblastoma.
6. The use according to claim 4 or 5, wherein the medicament is capable of inhibiting the expression of CEP89.
7. The use of claim 6, wherein the medicament comprises interfering RNA, a gene knockout agent, or a chemical inhibitor.
8. A pharmaceutical composition for preventing and/or treating neuroblastoma, wherein the pharmaceutical composition is capable of inhibiting the expression of CEP89.
9. The pharmaceutical composition of claim 8, wherein the pharmaceutical composition comprises a small interfering RNA that is targeted to inhibit CEP89.
10. A small interfering RNA for targeted inhibition of CEP89, which is characterized in that the nucleotide sequence of the small interfering RNA is shown as SEQ ID NO. 1;
and/or the nucleotide sequence of the small interfering RNA is shown as SEQ ID NO. 2.
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Cited By (2)
| Publication number | Priority date | Publication date | Assignee | Title |
|---|---|---|---|---|
| CN117568347A (en) * | 2024-01-15 | 2024-02-20 | 首都医科大学附属北京儿童医院 | Application of PPEF1 as neuroblastoma drug target |
| CN117582506A (en) * | 2024-01-17 | 2024-02-23 | 首都医科大学附属北京儿童医院 | Application of transmembrane protein TMEFF1 inhibitor in preparation of medicine for treating neuroblastoma |
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2023
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Cited By (4)
| Publication number | Priority date | Publication date | Assignee | Title |
|---|---|---|---|---|
| CN117568347A (en) * | 2024-01-15 | 2024-02-20 | 首都医科大学附属北京儿童医院 | Application of PPEF1 as neuroblastoma drug target |
| CN117568347B (en) * | 2024-01-15 | 2024-04-02 | 首都医科大学附属北京儿童医院 | Application of PPEF1 as neuroblastoma drug target |
| CN117582506A (en) * | 2024-01-17 | 2024-02-23 | 首都医科大学附属北京儿童医院 | Application of transmembrane protein TMEFF1 inhibitor in preparation of medicine for treating neuroblastoma |
| CN117582506B (en) * | 2024-01-17 | 2024-04-02 | 首都医科大学附属北京儿童医院 | Application of transmembrane protein TMEFF1 inhibitor in preparation of medicine for treating neuroblastoma |
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