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LINC00894 targets Annexin A2 to regulate oxaliplatin resistance in hepatocellular carcinoma: ANXA2 protein function
Junling Huang1, Jiajie Lin2, Tengmeng Zhong3
1The First Clinical Medical College of Jinan University, Guangzhou, Guangdong 530632, China; Department of Gastroenterology, Affiliated Hospital of Youjiang Medical University for Nationalities, Baise 533000, Guangxi Province, China; Guangxi Clinical Medical Research Center for Hepatobiliary Diseases, Baise, Guangxi 533000, China.
Abstract:
To investigate the role of LINC00894 in oxaliplatin chemoresistance of hepatocellular carcinoma (HCC) and its mechanisms. The oxaliplatin-resistant HCC cell lines were established. IC50 of oxaliplatin was calculated by CCK-8 assay. Cell viability was detected using clonal formation experiment, while cell apoptosis was accessed by flow cytometry. RNA binding protein immunoprecipitation and RNA pull-down were performed to explore the interaction of LINC00894 and ANXA2. The expressions of RNA and protein were tested by qRT-PCR and western blot respectively. Tumor xenograft was performed to detect the effect of LINC00894 in vivo. The expression of ki67 was evaluated by immunohistochemistry staining. LINC00894 was overexpressed in HCC cells resistant to oxaliplatin. Elevated LINC00894 promoted HCC cells resistance to oxaliplatin, whereas silence of LINC00894 improved HCC sensitivity to oxaliplatin. LINC00894 could bind to the ANXA2 protein, enhanced the stability of the ANXA2 protein and reduced its ubiquitination. Furthermore, LINC00894 modulated HCC resistance to oxaliplatin both in vitro and in vivo by targeting the ANXA2 protein.LINC00894 enhanced the stability of ANXA2 protein and attenuated its ubiquitination by interacting with it, thereby promoting oxaliplatin resistance in HCC. Our findings contributed to understanding the role of these mechanisms in the process of oxaliplatin resistance in HCC.
Insights
Long non-coding RNA LINC00894 promotes hepatocellular carcinoma (HCC) resistance to oxaliplatin chemotherapy. It enhances ANXA2 protein stability, reducing its ubiquitination, which is crucial for chemoresistance in HCC.
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- Hepatocellular carcinoma (HCC) is a major global health concern.
- Oxaliplatin is a key chemotherapeutic agent for HCC, but resistance limits its efficacy.
- Understanding mechanisms of oxaliplatin resistance is critical for improving HCC treatment.
Purpose of the Study:
- To investigate the role of LINC00894 in oxaliplatin chemoresistance in HCC.
- To elucidate the underlying molecular mechanisms of LINC00894-mediated chemoresistance.
Main Methods:
- Establishment of oxaliplatin-resistant HCC cell lines.
- Cell viability assays (CCK-8, clonal formation), apoptosis analysis (flow cytometry).
- RNA immunoprecipitation, RNA pull-down, qRT-PCR, Western blot, and in vivo tumor xenograft models.
Main Results:
- LINC00894 was significantly overexpressed in oxaliplatin-resistant HCC cells.
- Overexpression of LINC00894 conferred oxaliplatin resistance, while its silencing restored sensitivity.
- LINC00894 directly binds to ANXA2 protein, enhancing its stability and reducing its ubiquitination.
Conclusions:
- LINC00894 plays a critical role in promoting oxaliplatin chemoresistance in HCC.
- The LINC00894/ANXA2 interaction modulates HCC chemoresistance both in vitro and in vivo.
- Targeting LINC00894 may represent a novel therapeutic strategy for overcoming oxaliplatin resistance in HCC.
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