The long non-coding RNA LINC00473 contributes to cell proliferation via JAK-STAT3 signaling pathway by regulating miR-195-5p/SEPT2 axis in prostate cancer
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Updated: Dec 20, 2025

Laser-capture Microdissection of Human Prostatic Epithelium for RNA Analysis
Published on: November 26, 2015
Zengshu Xing1, Sailian Li2, Zhenxiang Liu1
1Department of Urology, Affiliated Haikou Hospital of Xiangya Medical College, Central South University, No.43, Renmin Road, Meilan District, Haikou, 570208, Hainan Province, P.R. China.
Abstract:
Prostate cancer is a kind of male malignant tumor, which has brought tremendous health threat to men. Prostate cancer is difficult to be cured because of high incidence and metastasis rate. Thereby, it is of great urgency to elucidate the underlying molecular mechanism of prostate cancer for the treatment of this cancer. LINC00473 dysregulation has been observed in many cancers. However, the role of LINC00473 was unknown in prostate cancer. In the present study, we discovered that prostate cancer cells presented high expression of LINC00473, and LINC00473 inhibition limited cell proliferation and the expression of proteins in JAK-STAT3 signaling pathway. Additionally, LINC00473 acted as an up-stream factor for miR-195-5p to negatively modulate miR-195-5p expression. Moreover, SEPT2 interacted with miR-195-5p in prostate cancer and SEPT2 expression was positively modulated by LINC00473 and negatively regulated by miR-195-5p. Last, the inhibitory effect of LINC00473 knockdown on cell proliferation and expression of proteins of JAK-STAT3 signaling pathway was restored by SEPT2 overexpression. All in all, LINC00473 contributed to cell proliferation via JAK-STAT3 signaling pathway by regulating miR-195-5p/SEPT2 axis in prostate cancer, which provided a novel therapeutic tactic for prostate cancer patients.
Insights
Long non-coding RNA LINC00473 promotes prostate cancer cell proliferation by regulating the miR-195-5p/SEPT2 axis and JAK-STAT3 pathway. Inhibiting LINC00473 offers a potential therapeutic strategy for prostate cancer.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Prostate cancer poses a significant health threat due to high incidence and metastasis.
- Understanding the molecular mechanisms of prostate cancer is crucial for effective treatment.
- LINC00473, a long non-coding RNA, has known roles in various cancers, but its function in prostate cancer was unclear.
Purpose of the Study:
- To investigate the role of LINC00473 in prostate cancer.
- To elucidate the molecular mechanism by which LINC00473 influences prostate cancer progression.
- To explore LINC00473 as a potential therapeutic target for prostate cancer.
Main Methods:
- Quantitative real-time PCR to measure LINC00473 expression.
- Cell proliferation assays to assess the impact of LINC00473.
- Western blotting to detect protein expression in the JAK-STAT3 pathway.
- RNA immunoprecipitation and dual-luciferase reporter assays to confirm molecular interactions.
Main Results:
- Prostate cancer cells exhibited high expression of LINC00473.
- LINC00473 inhibition suppressed cell proliferation and JAK-STAT3 signaling.
- LINC00473 negatively regulated miR-195-5p, which in turn regulated SEPT2.
- SEPT2 overexpression rescued the inhibitory effects of LINC00473 knockdown.
Conclusions:
- LINC00473 promotes prostate cancer cell proliferation through the JAK-STAT3 signaling pathway.
- The LINC00473/miR-195-5p/SEPT2 axis is a key regulatory mechanism in prostate cancer.
- Targeting LINC00473 presents a novel therapeutic avenue for prostate cancer treatment.
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