CN112691195B - Application of PRPF8 expression inhibitor in preparation of medicine for treating lung cancer - Google Patents
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Abstract
An application of a PRPF8 expression inhibitor in preparing a medicament for treating lung cancer, and belongs to the technical field of biology, in particular to an application of a PRPF8 expression inhibitor in preparing a medicament for treating lung cancer. The research of the invention finds that the cell growth can be inhibited and the cell clonogenic capacity can be inhibited by knocking down PRPF8 in the non-small cell lung cancer cell line, so that the PRPF8 in the non-small cell lung cancer can be used as a novel inhibitor for clinically treating the non-small cell lung cancer.
Description
Technical Field
The invention relates to the technical field of biology, in particular to application of a PRPF8 expression inhibitor in preparation of a medicine for treating lung cancer.
Background
Lung cancer is a common malignancy, and non-small cell lung cancer (NSCLC) is one of the lung cancers, accounting for about 80% -85%, second only to female breast cancer. The treatment scheme of the non-small cell lung cancer mainly comprises chemotherapy. Cisplatin remains by far the most widespread first-line chemotherapeutic agent for the treatment of NSCLC. However, the therapeutic effect is not significant, and the fundamental reason is that the target gene is not searched for from the source of the protein production.
The PRPF8 protein is about 280kDa, which is the center of the assembly kinetics of the U5 snRNP spliceosome. It makes direct contact not only with the 5 'branch point in the RNA substrate but also with the polypyrimidine tract in the 3' cleavage site. And simultaneously, the composition of U5 and U6snRNAs is also involved. In human autosomal dominant retinitis heria, PRPF8 is found to produce mutations that affect the assembly and function of the splice, causing localized disease, resulting in cytopenia.
At present, no relevant report is found on the function of PRPF8 in the occurrence, migration and invasion of lung cancer.
Disclosure of Invention
The invention aims to provide application of a PRPF8 expression inhibitor in preparing a medicament for treating lung cancer.
The invention relates to an application of a PRPF8 expression inhibitor in preparing a medicament for treating lung cancer.
Preferably, the lung cancer is non-small cell lung cancer.
Further, the PRPF8 expression inhibitor includes at least one of:
a compound that specifically inhibits the expression of PRPF 8;
an interfering molecule that specifically interferes with the expression of PRPF 8;
an antibody or ligand that specifically binds to a PRPF8 protein.
A PRPF8 gene-knockdown agent, said PRPF8 gene-knockdown agent being a gene-editing agent that specifically knockdown PRPF 8.
Further, the interfering molecule is miRNA or siRNA.
Further, the PRPF8 gene knock-down reagent comprises an expression vector, wherein the expression vector comprises a DNA coding sequence of shRNA segment, and the target gene of the shRNA segment is PRPF8 gene.
Preferably, the sequence of the shRNA fragment is shown as SEQ ID NO:1 is shown.
Preferably, the expression vector is a plasmid vector or a viral vector.
The invention also provides a medicament for treating lung cancer, which comprises a PRPF8 gene knockdown reagent, wherein the PRPF8 gene knockdown reagent comprises a shRNA fragment, and the target gene of the shRNA fragment is the PRPF8 gene.
Preferably, the sequence of the shRNA fragment is shown as SEQ ID NO:1 is shown.
Preferably, the lung cancer is non-small cell lung cancer.
The invention also provides application of the reagent in preparation of a kit, wherein the reagent is used for quantitatively detecting the PRPF8 protein expression level, and the kit is used for judging the effectiveness of the medicament in treating lung cancer.
Preferably, the lung cancer is non-small cell lung cancer.
The invention has the beneficial effects that:
the loss-of-function mutation of human PRPF8 delays the assembly of the pre-mRNA by the spliceosome components, inhibits the splicing of 9% (5/57) of the tested gene, generates functionally different proteins and plays an important role in the occurrence of diseases and the growth of tumors.
According to the invention, the growth of cells can be inhibited and the cell clonogenic capacity can be inhibited by knocking down PRPF8 in the non-small cell lung cancer cell line, so that PRPF8 in the non-small cell lung cancer can be used as a novel inhibitor for clinically treating the non-small cell lung cancer.
The cell growth of the non-small cell lung cancer can be inhibited by inhibiting the expression quantity of the gene, and the gene can become a medicament for clinically treating the non-small cell lung cancer.
Drawings
FIG. 1 shows the result of fluorescence identification of knockdown cell lines;
FIG. 2 shows the WB identification result of PRPF8 knockdown cell line;
FIG. 3 is the results of a KEGG enrichment analysis;
FIG. 4 shows the results of the cell growth curve of A549 knockdown PRPF8 cells;
FIG. 5 shows the result of cloning A549 knockdown PRPF8 cells;
FIG. 6 is imageJ analysis the clone formation results of FIG. 5;
FIG. 7 is a MDA-MB-468 knockdown PRPF8 cell growth curve;
FIG. 8 shows the result of clone formation of MDA-MB-468 cells knocking down PRPF 8;
figure 9 is imageJ analysis figure 8 results of clone formation.
Detailed Description
The following examples are given to illustrate the present invention, and the following examples are carried out on the premise of the technical solution of the present invention, and give detailed embodiments and specific procedures, but the scope of the present invention is not limited to the following examples.
Example 1 bioinformatics analysis of PRPF8 expression in Lung cancer
The expression of PRPF8 in lung cancer is analyzed by utilizing a database, the PRPF8 is subjected to enrichment analysis by utilizing databases such as KEGG and the like, a PRPF8 regulation and control pathway in the lung cancer is concerned, and a main action pathway of the PRPF8 in the lung cancer is analyzed.
Example 2 establishment of knockdown cell lines
2 shRNAs were synthesized based on the PRPF8 sequence design and ligated into p-GIPZ and p-TRIPZ vectors (purchased from Addgene Biotechnology Ltd., USA) as shown in the following table.
Table shRNA sequences
Example 3 Lentiviral preparation
(1) Inoculating 293T cells into a 25cm small bottle, culturing overnight, then removing the culture medium, and replacing 2.5mL of DMEM non-resistant culture medium;
(2) Plasmids pPAX2, pMD2, GIPZ-CTRL; plasmids pPAX2, pMD2, GIPZ-PRPF8-1; uniformly mixing the plasmids pPAX2, pMD2 and GIPZ-PRPF8-4, adding 250 mu L of opti-MEM culture medium, then diluting Lipo2000 with 250 mu L of opti-MEM culture medium, standing at room temperature for 5min, mixing the plasmids with the Lipo2000, standing at room temperature for 20min, and adding into 293T cells;
(3)5％CO 2 changing a DMEM culture medium after culturing for 18 hours;
(4) Culturing for 48h, recovering supernatant, and filtering with 0.45 μ M filter membrane;
(5) Adding 1/3 volume of virus concentrated solution (25% PEG8000/0.75M NaCl), mixing, and standing at 4 deg.C overnight;
(6) Then centrifuging at 4 ℃ and 1500g for 45min, discarding the supernatant, dissolving the precipitate with 1640 culture medium to obtain virus supernatants of GIPZ-CTRL, GIPZ-PRPF8-1 and GIPZ-PRPF8-4 respectively. Subpackaging and storing at-80 deg.C.
Example 4 transfection of cells
(1) Screening for purine concentration
A549 cell line was digested with pancreatin for 3 minutes, resuspended in a single cell suspension with medium, and cell density was adjusted to 10 per well 5 After culturing for 30 hours, the cells are changed into culture media containing purine at different concentrations, and the final concentrations are respectively: 0.25. Mu.g/ml, 0.4. Mu.g/ml, 0.6. Mu.g/ml, 0.75. Mu.g/ml, 1.0. Mu.g/ml, and the culture was continued for 7 days with the liquid change every 24 hours, and the concentration of cell death, that is, the optimum puromycin concentration was observed.
(2) Viral transfection
A549 cells were seeded in 6-well plates at 2X 10 cells per well 5 Culturing the cells overnight; after 24h, the culture medium is discarded, washed once by PBS, and 1.2mL of fresh culture medium containing no antibody and serum and containing polybrene is added; adding GIPZ-CTRL, GIPZ-PRPF8-1 and GIPZ-PRPF8-4 virus supernatants; centrifuging at 2000rpm at 32 ℃ for 1h;37 ℃ 5% of CO 2 After culturing for 5h, 1mL of complete culture medium was added to each well; after 24h of culture, the culture medium is discarded, and a fresh culture medium containing puromycin (the final concentration is 0.75 mu g/mL) is added, and the culture medium is changed every three days; after 5 days of culture, the cells were harvested and RNA was extracted.
Example 5, q-PCR identification
Cells were seeded in 6-well plates at 2X 10 per well 5 And (3) culturing the cells overnight, then removing the culture medium, adding a fresh medium containing puromycin, changing the culture medium once a day, collecting the cells after 3 consecutive days, and extracting RNA and performing reverse transcription to obtain cDNA. q-PCR was performed.
The q-PCR reaction system is as follows:
real-time quantitative PCR reaction procedure: pre-denaturation at 94 ℃ for 5min,95 ℃ for 10sec,60 ℃ for 2 sec,72 ℃ for 10sec for 40 cycles.
Example 6 cell proliferation assay
A549 cells 6-well plate inoculated with 2X 10 cells per well 5 Adding GIPZ-CTRL, GIPZ-PRPF8-1 and GIPZ-PRPF8-4 viruses and puromycin 0.75 mu g/mL for 5 days, collecting cells, inoculating to 96-well plate with each well being 1X 10 4 Each cell line was plated in 6 duplicate wells and cultured for 7 days, and the OD was measured daily using CCK8 kit.
Example 7 cell clone formation experiment
A549 cells 6-well plate inoculated with 2X 10 cells per well 5 Adding GIPZ-CTRL, GIPZ-PRPF8-1 and GIPZ-PRPF8-4 viruses into each well, screening puromycin for 5 days, adjusting the cell number, inoculating 500 cells into each well of a 6-well plate, repeating 3 samples of each cell line, culturing for 7 days, discarding the culture medium, washing the cells with PBS for 2 times, adding 1mL of methanol into each well for fixing the cells for 20min, discarding methanol, washing with PBS for 2 times, adding 1mL of 1% crystal violet solution into each well, dyeing for 20min at room temperature, washing with PBS for 2 times, and ddH 2 Wash once and take pictures with gel imaging system.
In order to verify that the inhibition effect of PRPF8 on the growth of lung cancer cells is limited to an action mechanism in the lung cancer cells, the virus prepared by the same method and the same batch is adopted to infect breast cancer MDA-MB-468 cells, and the growth capacity of PRPF8 detection cells is knocked down in the breast cancer cells.
The fluorescence identification result of the knockdown cell line is shown in figure 1, and TRIPZ-shCTRL doxycline induction is carried out for 72h on the left side; the middle part is TRIPZ-shPRPF8-1 Doxycyline induced 72h, and the right side is TRIPZ-shPRPF8-4 Doxycyline induced 72h. The WB identification results of the PRPF8 knockdown cell line are shown in fig. 2.
The detection results show that:
1. fig. 3 is a KEGG enrichment analysis result, and analysis of KEGG on PRPF8 expression in lung cancer shows that PRPF8 is closely related to multiple pathways in lung cancer, including a PI3K-Akt signaling pathway, cisplatin resistance, small cell lung cancer, homologous recombination, and the like, among which the PI3K-Akt signaling pathway is the most significant, and the PI3K-Akt signaling pathway is a typical cell growth regulatory pathway and regulates a cell growth pathway, thereby suggesting that PRPF8 is related to the growth of lung cancer cells.
2. To investigate the role of PRPF8 in non-small cell lung cancer, we established a PRPF8 knockdown cell line in a549 cells. p-TRIPZ-shPRPF8-1, p-TRIPZ-shPRPF8-4 and p-RIPZ-shCTRL lentivirus transfect A549 cells, puromycin 0.75 mu g/mL is screened for 5 days, cell RNA extraction is collected, and the PRPF8mRNA expression in cell lines of A549-TRIPZ-PRPF8-1, A549-TRIPZ-PRPF8-4 and A549-TRIPZ-CTRL is reduced by 1.5 times and 1.63 times through qPCR detection.
3. Knockdown PRPF8 inhibits growth of A549 cells
In order to verify the effect of PRPF8 in the growth of lung cancer cells, a CCK-8 kit is used for detecting the proliferation of cells in a knockdown cell line constructed by A549 cells, 1% crystal violet is used for dyeing and observing the clonogenic capacity of the cells, and the result shows that after the A549 cells are knocked down and PRPF8 is knocked down, the cell proliferative capacity is inhibited, the clonogenic capacity of the cells is declined (p is less than 0.05) after the A549 cells are knocked down and PRPF8 is knocked down, apoptotic cells are increased, and the cells grow slowly.
The cell growth curve of A549 knockdown PRPF8 is shown in FIG. 4, wherein the expression curve is 9632CTRL and 9679798-1, and the expression curve is PRPF8-4. Silencing PRPF8 in a549 cells significantly reduced the ability of the cells to clonally form.
The cloning formation result of a549 knockdown PRPF8 cells is shown in fig. 5, and the cloning formation ability of cells is reduced after the PRPF8 is knocked down in a549 cells.
Clone formation results of imageJ analysis are shown in fig. 6, and shPRPF8 cell clone formation ability was significantly reduced (p < 0.05) after PRPF8 was knocked down.
4. PRPF8 knockdown in breast cancer cell lines
The MDA-MB-468 cell growth curve for knocking down PRPF8 is shown in FIG. 7, wherein diamond-solid in FIG. 7 represents CTRL, \ 9632while PRPF8-1 and tangle-solidup represents PRPF8-4. The results of clone formation of MDA-MB-468 cells knocking down PRPF8 are shown in FIG. 8. The results of imageJ analysis clone formation are shown in fig. 9.
After PRPF8 is knocked down in the MDA-MB-468 breast cancer cell line, a cell growth curve is monitored for 5 days, and the result shows that compared with a control group, the cell growth of a PRPF8 knocking down group is not different (p is greater than 0.05), and the cell clone forming capability of the knocking down group is not remarkably reduced (p is greater than 0.05) in a cell clone forming test, so that the capability of PRPF8 for regulating the cell growth is proved to be specific in lung cancer and not have the same regulating capability in other cancers. Each cancer has different pathogenic organs, different mechanisms and different regulatory pathways in cancer cells, so that the regulation has organ heterogeneity and tumor heterogeneity.
5. To further demonstrate that the ability of PRPF8 to regulate cell growth in lung cancer is unique, we analyzed the expression and enrichment of PRPF8 in breast cancer using a database, and found that PRPF8 is closely related to multiple pathways, among which PRPF8 has significant association with 9 pathways (p-value < 0.05), and these 9 pathways are involved in 9 aspects of regulation, such as ribosome, oxidative stress, parkinson's syndrome, myocardial contraction, huntington's syndrome, senile dementia, metabolism of p450, and proteasome, but not related to cell growth regulation.
The experimental results obtained from the above prove that the knockout of PRPF8 in non-small cell lung cancer can inhibit the growth of cancer cells, so that the inhibitor aiming at the synthesis of PRPF8 can effectively inhibit the growth of cancer cells in vivo, reduce the survival of tumor cells, and is a clinically effective therapeutic drug.
Claims (6)
- The application of PRPF8 expression inhibitor in preparing medicine for treating lung cancer; the lung cancer is non-small cell lung cancer A549.
- 2. Use according to claim 1, characterized in that the inhibitor of PRPF8 expression comprises at least one of:a compound that specifically inhibits the expression of PRPF 8;an interfering molecule that specifically interferes with the expression of PRPF 8;an antibody or ligand that specifically binds to a PRPF8 protein;a PRPF8 gene-knockdown agent, said PRPF8 gene-knockdown agent being a gene-editing agent that specifically knockdown PRPF 8.
- 3. The use according to claim 2, wherein the PRPF8 gene knockdown agent comprises an expression vector comprising the DNA coding sequence of an shRNA fragment whose target gene is the PRPF8 gene.
- 4. Use according to claim 3, characterized in that the sequence of the shRNA fragment is represented by the sequences PRPF8-1 and PRPF8-4.
- 5. Use according to claim 3, characterized in that the expression vector is a plasmid vector or a viral vector.
- 6. The application of the reagent in the preparation of the kit is characterized in that the reagent is used for quantitatively detecting the PRPF8 protein expression level, the kit is used for judging the effectiveness of the medicament in treating the lung cancer, and the lung cancer is non-small cell lung cancer A549.
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