@Article{or.2023.030771,
AUTHOR = {XIAOBI HUANG, CHUNYUAN CHEN, YONGYANG CHEN, HONGLIAN ZHOU, YONGHUA CHEN, ZHONG HUANG, YULIU XIE, BAIYANG LIU, YUDONG GUO, ZHIXIONG YANG, GUANGHUA CHEN, WENMEI SU},
TITLE = {Silencing of the long non-coding RNA <i>LINC00265</i> triggers autophagy and apoptosis in lung cancer by reducing protein stability of SIN3A oncogene},
JOURNAL = {Oncology Research},
VOLUME = {32},
YEAR = {2024},
NUMBER = {7},
PAGES = {1185--1195},
URL = {http://www.techscience.com/or/v32n7/57163},
ISSN = {1555-3906},
ABSTRACT = { <b>Background:</b> Long 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. <i>LINC00265</i> 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. <b>Methods:</b> Here, the regulatory role of <i>LINC00265</i> in lung adenocarcinoma was examined using lung cancer cell lines, clinical samples, and xenografts. <b>Results:</b> We found that high levels of <i>LINC00265</i> expression were associated with shorter overall survival rate of patients, whereas knockdown of <i>LINC00265</i> inhibited proliferation of cancer cell lines and tumor growth in xenografts. Western blot and flow cytometry analyses indicated that silencing of <i>LINC00265</i> induced autophagy and apoptosis. Moreover, we showed that <i>LINC00265</i> 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 <i>LINC00265</i> functions to promote the oncogenic activity of SIN3A in lung adenocarcinoma. <b>Conclusions:</b> Our findings thus identify SIN3A as a <i>LINC00265</i>-associated protein and should help to understand the mechanism underlying <i>LINC00265</i>-mediated oncogenesis.},
DOI = {10.32604/or.2023.030771}
}