Study suggests miR-377 as potential therapeutic target for prostate cancer

A new research paper was published in Genes & Cancer on May 16, 2024, 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."

The MYC gene is a regulatory and proto-oncogenic gene that is overexpressed in the majority of prostate cancers (PCa). Numerous studies have indicated that aberrant expression of microRNAs is involved in the initiation and progression of prostate cancer. In this new study, researchers Yasamin Azimi, Sara Hajibabaei, Ghazal Azimi, Fatemeh Rahimi-Jamnani, and Masoumeh Azizi from the Pasteur Institute of Iran and Islamic Azad University assessed the impact of miR-377 on MYC through luciferase assay. 

"[...] it is of utmost importance to conduct research on the molecular pathways underlying the progression of PCa, as this may potentially lead to the development of a novel approach for targeted treatment of the disease."

Real-time PCR was employed to determine whether miR-377 could reduce the levels of MYC mRNA in transfected PCa cell lines (PC-3 and DU145) and change in the mRNA levels of BCL-2/Bax, PTEN, and CDK4 as a consequence of MYC downregulation. Moreover, the researchers analyzed the effects of miR-377 on apoptosis, proliferation, cell cycle, and wound healing. 

Their findings demonstrate that miR-377 effectively targets MYC mRNA, as confirmed by luciferase assay and Real-time PCR. They observed a significant reduction in BCL-2 and CDK4 expression, along with an increase in Bax and PTEN, in prostate cancer cell lines upon MYC suppression. Additionally, elevated levels of miR-377 in PCa cell lines induced apoptosis, inhibited proliferation and migration, and arrested the cell cycle.

"Taken together, these results unveil the inhibitory role of miR-377 in MYC function within PCa, thereby suggesting its potential as a therapeutic target for the treatment of this malignancy."