The MYC gene is a regulatory and proto-oncogene that is overexpressed in most prostate cancers (PCa). A large number of research results have shown that abnormal expression of microRNAs is involved in the occurrence and progression of human prostate cancer. Recently, in a research report entitled "Inhibitory effect of miR-377 on the proliferative and invasive behaviors of prostate cancer cells through the modulation of MYC mRNA via its interaction with BCL-2/Bax, PTEN, and CDK4" published in the international journal Genes & Cancer, scientists from the Pasteur Institute of Iran and other institutions revealed the inhibitory effect of miR-377 on prostate cancer cells through research.
In the article, the researchers evaluated the effect of miR-377 on MYC by luciferase assay. They believe that in-depth research on the molecular pathways behind the progression of prostate cancer is very necessary, which may help develop targeted therapies for this disease. The researchers used real-time PCR to determine whether miR-377 could reduce the level of MYC mRNA in transfected prostate cancer cell lines (PC-3 and DU145) and whether the downregulation of MYC would lead to changes in the levels of BCL-2/Bax, PTEN, and CDK4. In addition, the researchers analyzed the effects of miR-377 on cell apoptosis, proliferation, cell cycle, and wound healing.
Figure 1. miR-377 transfection in prostate cancer cell lines can target MYC 3'UTR, degrade its mRNA, and affect cell apoptosis, cell cycle, migration, and cell proliferation.
The BCL-2 protein is responsible for regulating apoptosis and its function is to penetrate the mitochondrial membrane and act as a potent inhibitor of the apoptotic process. The interaction between BCL-2 and the pro-apoptotic component Bax leads to the formation of heterodimers. This contact between the two proteins leads to the elimination of the pro-apoptotic properties of Bax. Therefore, the occurrence of apoptosis depends on the ratio of BCL-2/Bax. It was observed that the introduction of miR-377 led to a significant decrease in the presence of BCL-2 mRNA in PC-3 and DU145 prostate cancer cells. Conversely, exposure of these cells to miR-377 led to an increase in Bax protein expression. This result suggests that the ratio of Bax to BCL-2 shifted in the direction of apoptosis due to the decrease in MYC mRNA levels.
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The study found that transfection of miR-377 in prostate cancer cell lines led to a decrease in MYC expression, while the decrease in MYC mRNA levels led to an increase in PTEN mRNA levels, and therefore the survival and proliferation rates of prostate cancer cell lines were reduced. Overexpression of the MYC gene can lead to upregulation of CDK4 expression, which promotes cell cycle progression and cell division. Transfection of miR-377 resulted in cell cycle arrest in prostate cancer cell lines, which was due to decreased MYC mRNA expression levels, which in turn led to decreased CDK4 mRNA expression levels.
The effects of miR-377 on cell growth, apoptosis, and cell cycle were evaluated by MTT assay and flow cytometry. The results showed that miR-377 significantly impeded cell proliferation, induced apoptosis, arrested the cell cycle at the G0/G1 phase, and inhibited cell migration in PC-3 and DU145 cells compared with control and scrambled miRNA, suggesting that miR-377 may play a role in preventing prostate cancer by targeting MYC 3'UTR. These findings are consistent with earlier studies showing that miR-377 can inhibit the proliferation of lung cancer, hepatocellular carcinoma, human osteosarcoma, glioblastoma, and pancreatic cancer cells.
In summary, the results of this study revealed an inhibitory effect of miR-377 on MYC function in prostate cancer, which may indicate its potential as a target for the development of treatments for this malignancy.
Reference
Azimi Y, et al. Inhibitory effect of miR-377 on the proliferative and invasive behaviors of prostate cancer cells through the modulation of MYC mRNA via its interaction with BCL-2/Bax, PTEN, and CDK4. Genes & Cancer, 2024, 15: 28.