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(Slides)

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The study examines the role of the long non-coding RNA LINC00265 in lung adenocarcinoma. The researchers found that LINC00265 is upregulated in lung cancers and cell lines compared to noncancerous lung tissues. They also observed that the expression of LINC00265 can distinguish between normal and tumor tissues. Furthermore, they found that higher expression of LINC00265 is associated with poorer overall survival rates in lung cancer patients.<br /><br />To investigate the functional role of LINC00265, the researchers conducted experiments using lung cancer cell lines and xenografts. They demonstrated that silencing of LINC00265 inhibited the proliferation of lung cancer cells and reduced tumor growth in xenografts. They also found that knockdown of LINC00265 induced autophagy, a cellular process that promotes cell death.<br /><br />The study further investigated the mechanism underlying the role of LINC00265 in cancer progression. They found that LINC00265 interacts with the SIN3A protein, which is known to be involved in cancer development. Knockdown of LINC00265 resulted in reduced SIN3A protein levels and inhibited the migration and invasion of lung cancer cells. Additionally, knockdown of SIN3A also induced autophagy and increased apoptosis in lung cancer cells.<br /><br />Overall, the study suggests that LINC00265 plays a role in promoting lung cancer progression by stabilizing the SIN3A protein. Silencing of LINC00265 can inhibit cell proliferation, induce autophagy, and promote apoptosis in lung cancer cells. These findings provide insights into the potential use of LINC00265 as a therapeutic target for lung adenocarcinoma.

Asset Subtitle

wenmei su

Meta Tag

Speaker wenmei su

Topic Tumor Biology: Preclinical Biology - Regulatory Mechanisms

Keywords

LINC00265

lung adenocarcinoma

upregulated

expression

overall survival rates

proliferation

tumor growth

autophagy

SIN3A protein

therapeutic target