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Sandy Srinivas, MD


LINC00893: Does It Have a Novel Tumor-Suppressor Role to Play in Prostate Cancer?

By: Cordi Craig, MS
Posted: Tuesday, August 30, 2022

Previous studies have reported that long non-coding RNA LINC00893 may inhibit the proliferation and metastasis of papillary thyroid cancer cells, but its role in the treatment of prostate cancer remains unknown. Gang Guo, MD, of Chinese People’s Liberation Army General Hospital, Beijing, and colleagues investigated the underlying mechanisms of LINC00893 in regulating the progression of prostate cancer and suggest that LINC00893 may play an important role in targeted therapy for this genitourinary cancer. The report was published in Cancer Cell International.

“Our research enriches the molecular network of LINC00893 in regulating the progression of prostate cancer and provides a theoretical foundation for prostate cancer targeted therapy,” the study authors concluded.

Using The Cancer Genome Atlas, the study authors compared LINC00893 expression levels in prostate cancer tissues and normal prostate tissues. LINC00893 expression levels were validated in sample pairs (n = 66) of prostate cancer and paracancerous normal tissues as well as in prostate cancer cell lines. Several assays were performed to assess functional phenotypes and evaluate molecular interactions.

The investigators found that LINC00893 was downregulated in cancerous tissue and cell lines. Low expression of LINC00893 seemed to be associated with a poorer overall survival rate. The overexpression of LINC00893 restricted the proliferation, epithelial-mesenchymal transition, and migratory ability of prostate cancer cells. In addition, increased LINC00893 expression suppressed the tumorigenesis of prostate cancer cells in nude mice. Furthermore, the research team described the sponge-like qualities of LINC00893 for miR-3173-5p, which inhibited its activity. In turn, the inhibition of miR-3173-5p suppressed the cytokine signaling 3 (SOCS3)/Janus kinase 2 (JAK2)/signal transducer and activator of the transcription 3 signaling axis.

Disclosure: The study authors reported no conflicts of interest.

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