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Sequencing Small Non-coding RNA from Formalin-fixed Tissues and Serum-derived Exosomes from Castration-resistant Prostate Cancer Patients
Published on: November 19, 2019
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Long non-coding RNA AC245100.4 activates the PI3K/AKT pathway to promote PCa cell proliferation by elevating PAR2
Ke Zhang1, Chi Liu1, Changbin Hu1,2
1Department of Biochemistry & Molecular Biology, Harbin Medical University, Harbin, Heilongjiang, 150086, China.
Heliyon
|June 22, 2023
Summary
The long non-coding RNA AC245100.4 promotes prostate cancer cell proliferation by activating the PAR2/PI3K/AKT pathway. This finding identifies AC245100.4 as a potential therapeutic target for prostate cancer.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Prostate cancer (PCa) is a prevalent malignancy in males.
- The long non-coding RNA (lncRNA) AC245100.4 is implicated in PCa development.
- The precise mechanism of AC245100.4 in PCa remains unclear.
Purpose of the Study:
- To investigate the role of AC245100.4 in PCa cell proliferation.
- To elucidate the underlying molecular mechanisms of AC245100.4 in PCa.
Main Methods:
- Quantitative reverse transcription PCR (qRT-PCR) for AC245100.4 expression.
- RNA immunoprecipitation followed by mass spectrometry (RAP-MS) for pathway identification.
- Cell Counting Kit-8 and colony formation assays for proliferation.
- Western blotting for protein expression (PAR2, AKT, p-AKT, Cyclin D1, PCNA).
Main Results:
- AC245100.4 and PAR2 overexpression enhanced PCa cell proliferation; knockdown yielded opposite effects.
- PAR2 was identified as a direct downstream target of AC245100.4.
- AC245100.4 promotes PCa proliferation via the PI3K/AKT pathway.
- PAR2 knockdown reversed the effects of AC245100.4 overexpression on p-AKT levels.
Conclusions:
- AC245100.4 promotes PCa cell proliferation by regulating the PAR2/PI3K/AKT axis.
- AC245100.4 may serve as a novel tumor marker and therapeutic target for PCa.
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