ABALON regulates mitophagy and 5-FU sensitivity in colorectal cancer via PINK1-Parkin pathway
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View abstract on PubMed
Summary
This summary is machine-generated.Long non-coding RNA ABALON promotes colorectal cancer (CRC) progression by regulating mitophagy. Targeting ABALON may reverse chemoresistance, offering a new therapeutic strategy for CRC patients.
Area Of Science
- Molecular Biology
- Oncology
- Cell Biology
Background
- Long non-coding RNAs (lncRNAs) are implicated in colorectal cancer (CRC) chemoresistance.
- Mitophagy is crucial for tumor cell survival, but its regulation by lncRNAs in CRC remains unclear.
Purpose Of The Study
- To investigate the role of lncRNAs in regulating mitophagy and chemoresistance in colorectal cancer.
- To evaluate the specific function of apoptotic BCL2L1-antisense long non-coding RNA (ABALON) in CRC.
Main Methods
- Utilized gain/loss of function experiments to study ABALON's biological impact.
- Assessed mitophagy using Western blot and JC-1 probe.
- Determined 5-fluorouracil (5-FU) chemosensitivity via CCK-8, flow cytometry, colony formation, and transwell assays.
Main Results
- ABALON expression is elevated in CRC, correlating with advanced tumor stage and metastasis.
- ABALON knockdown inhibited proliferation and enhanced apoptosis; it also sensitized CRC cells to 5-FU.
- ABALON overexpression promoted proliferation, metastasis, and 5-FU resistance, linked to altered mitophagy.
Conclusions
- ABALON drives colorectal cancer progression through PINK1/Parkin-mediated mitophagy.
- ABALON represents a potential therapeutic target for overcoming 5-FU resistance in CRC.
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