@article{HUANG2024, 
author = {XIAOBI HUANG and CHUNYUAN CHEN and YONGYANG CHEN and HONGLIAN ZHOU and YONGHUA CHEN and ZHONG HUANG and YULIU XIE and BAIYANG LIU and YUDONG GUO and ZHIXIONG YANG and GUANGHUA CHEN and WENMEI SU},
title = {Silencing of the long non-coding RNA LINC00265 triggers autophagy and apoptosis in lung cancer by reducing protein stability of SIN3A oncogene},
year = {2024},
journal = {Oncology Research},
volume = {32},
number = {7},
pages = {1185-1195},
keywords = {LINC00265, Autophagy, Lung adenocarcinoma (LUAD), Cancer progression, Switch-independent 3a (SIN3A)},
url = {https://www.sciopen.com/article/10.32604/or.2023.030771},
doi = {10.32604/or.2023.030771},
abstract = {BackgroundLong non-coding RNAs are important regulators in cancer biology and function either as tumor suppressors or as oncogenes. Their dysregulation has been closely associated with tumorigenesis. LINC00265 is upregulated in lung adenocarcinoma and is a prognostic biomarker of this cancer. However, the mechanism underlying its function in cancer progression remains poorly understood.MethodsHere, the regulatory role of LINC00265 in lung adenocarcinoma was examined using lung cancer cell lines, clinical samples, and xenografts.ResultsWe found that high levels of LINC00265 expression were associated with shorter overall survival rate of patients, whereas knockdown of LINC00265 inhibited proliferation of cancer cell lines and tumor growth in xenografts. Western blot and flow cytometry analyses indicated that silencing of LINC00265 induced autophagy and apoptosis. Moreover, we showed that LINC00265 interacted with and stabilized the transcriptional co-repressor Switch-independent 3a (SIN3A), which is a scaffold protein functioning either as a tumor repressor or as an oncogene in a context-dependent manner. Silencing of SIN3A also reduced proliferation of lung cancer cells, which was correlated with the induction of autophagy. These observations raise the possibility that LINC00265 functions to promote the oncogenic activity of SIN3A in lung adenocarcinoma.ConclusionsOur findings thus identify SIN3A as a LINC00265-associated protein and should help to understand the mechanism underlying LINC00265-mediated oncogenesis.}
}