2023 World Conference on Lung Cancer (Posters)-EP02.03. Silencing of Long Non-coding RNA LINC00265 Triggers Autophagy in Lung Canerby Reducing Protein Stability ofSIN3A Oncogene

EP02.03. Silencing of Long Non-coding RNA LINC00265 Triggers Autophagy in Lung Canerby Reducing Protein Stability ofSIN3A Oncogene - PDF(Abstract)

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A study presented at the World Conference on Lung Cancer in 2023 investigated the role of a long non-coding RNA called LINC00265 in lung adenocarcinoma. The researchers found that high levels of LINC00265 expression were associated with a shorter overall survival rate in patients. They also observed that knocking down LINC00265 inhibited the proliferation of cancer cell lines and tumor growth in xenografts. Further analysis revealed that silencing LINC00265 induced autophagy and apoptosis in lung cancer cells. <br /><br />The study also identified a protein called SIN3A that interacts with and is stabilized by LINC00265. SIN3A is known to function as a tumor suppressor or oncogene depending on the context. Silencing SIN3A also reduced the proliferation of lung cancer cells and induced autophagy. <br /><br />Based on these findings, the researchers suggested that LINC00265 may promote the oncogenic activity of SIN3A in lung adenocarcinoma. This study provides new insights into the mechanism by which LINC00265 contributes to cancer progression in the lungs.<br /><br />Overall, this research highlights the importance of long non-coding RNAs in cancer biology and suggests that LINC00265 may serve as a prognostic biomarker and potential therapeutic target for lung adenocarcinoma. Further studies are needed to fully understand the role of LINC00265 and its interaction with SIN3A in cancer development and progression.

Asset Subtitle

wenmei su

Meta Tag

Speaker wenmei su

Topic Tumor Biology: Preclinical Biology - Regulatory Mechanisms

Keywords

World Conference on Lung Cancer

long non-coding RNA

LINC00265

lung adenocarcinoma

overall survival rate

cancer cell lines

tumor growth

autophagy

apoptosis

SIN3A