2023 World Conference on Lung Cancer (Posters)-EP02.03. Suppression of the Long Non-coding RNA LINC01279 Triggers Autophagy in Lung Cancer by Regulating SIN3A

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Lung cancer is a deadly disease, and understanding the molecular mechanisms involved in its development is crucial for developing new diagnostic and therapeutic strategies. Long non-coding RNAs (lncRNAs) have been found to play important roles in the progression of lung cancer. One particular lncRNA, called LINC01279, has been found to be dysregulated in lung cancer, but its exact role in tumorigenesis is still unclear.<br /><br />In this study, the researchers aimed to explore the function of LINC01279 in lung adenocarcinoma (LUAD) using clinical samples, cell lines, and animal models. They found that LINC01279 was significantly upregulated in LUAD tissues and cell lines compared to noncancerous tissues. High expression of LINC01279 was also associated with poor overall survival rates in patients.<br /><br />Further experiments revealed that knockdown of LINC01279 inhibited tumor progression and promoted apoptosis in lung cancer cells. Knockdown of LINC01279 led to reduced cell proliferation, migration, and invasion, as well as increased apoptosis in lung cancer cell lines and xenografts.<br /><br />The researchers also investigated the molecular mechanisms underlying the role of LINC01279 in lung cancer. They discovered that LINC01279 interacts with and stabilizes a protein called SIN3A, which is involved in regulating gene expression. Knockdown of SIN3A also led to reduced cell proliferation, migration, and invasion in lung cancer cells.<br /><br />Additionally, the researchers found that LINC01279 regulates the activity of FAK and ERK, proteins that are involved in cell proliferation and migration. Knockdown of LINC01279 led to reduced levels of FAK and phosphorylated ERK, indicating that LINC01279 may promote lung cancer cell invasion by regulating these proteins.<br /><br />In conclusion, this study provides valuable insights into the role of LINC01279 in lung cancer. It demonstrates that LINC01279 is upregulated in LUAD and promotes tumor progression by regulating FAK and ERK. The study also reveals an interaction between LINC01279 and SIN3A, which may contribute to the survival of lung cancer cells. These findings highlight LINC01279 as a potential diagnostic and therapeutic target in lung cancer.

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wenmei su

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Speaker wenmei su

Topic Tumor Biology: Preclinical Biology - Regulatory Mechanisms

Keywords

Lung cancer

molecular mechanisms

LINC01279

tumorigenesis

LUAD

tumor progression

apoptosis

cell proliferation

cell migration

SIN3A