Dataset Information

Overexpression of BCCIP predicts an unfavorable prognosis and promotes the proliferation and migration of lung adenocarcinoma.

ABSTRACT:

Background

Lung cancer accounts for the highest rate of cancer-related diagnosis and mortality. Lung adenocarcinoma (LUAD) is the most common histopathological type. BCCIP was originally identified as a BRCA2 and CDKN1A interacting protein. In different cancers, BCCIP plays different roles. The role of BCCIP in LUAD is still unknown.

Methods

The expression and prognostic value of BCCIP was analyzed using public databases, including LCE, GEPIA, TCGA, and clinical specimens. Bioinformatic analysis and vitro experiments were conducted to explore the biological functions of BCCIP in LUAD. By using the GEPIA and TIMER databases, we investigated the correlations between LUAD expression and immune infiltration in LUAD.

Results

Compared with normal tissue, LUAD tissue had a higher expression level of BCCIP and high expression level of BCCIP was detrimental to LUAD patient survival. The suppression of BCCIP inhibited LUAD cell proliferation, migration and resulted in G1/S phase arrest in vitro. Bioinformatic analysis demonstrated that BCCIP could be associated with cell cycle, DNA repair and E2F transcription factor family. There were significant correlations between BCCIP expression and immune infiltrates, including B cell, CD4+ T cell, macrophage, neutrophil and dendritic cells. Furthermore, BCCIP expression showed strong correlations with diverse immune marker sets in LUAD, such as B cell, macrophage and DC.

Conclusions

Overexpression of BCCIP predicts an unfavorable prognosis and promotes the proliferation and migration of lung adenocarcinoma cells. BCCIP is correlated with immune infiltration in LUAD. Suppression of BCCIP may be a potential approach in the prevention and treatment of LUAD.

SUBMITTER: Shi J

PROVIDER: S-EPMC8410572 | biostudies-literature |

REPOSITORIES: biostudies-literature

ACCESS DATA

Similar Datasets

Project description:Background: The long non-coding RNA Linc00152 stimulates tumor progression in cancer. However, its clinical significance and biological functions in lung adenocarcinoma remains unknown. We evaluate the expression of Linc00152 in lung adenocarcinoma and its possible correlation with clinicopathologic features and patient survival to reveal its biological effects in cancer progression and prognosis. Methods: Total RNA extraction was performed on 110 pairs of lung adenocarcinoma and adjacent normal tissue samples, and then RT-qPCR was conducted. Chi-square test analysis was used to calculate the correlation between pathological parameters and the Linc00152 mRNA levels. Kaplan-Meier and Cox proportional hazards analyses were used to analyze the overall survival (OS) and disease-free survival (DFS) rates. We also detected the potential functional effects of overexpression and knockdown of Linc00152 in vitro cell proliferation, tumor cell invasion and migration, as well as in vivo nude mouse xenograft and metastasis models. Results: The Linc00152 expression levels were higher in lung adenocarcinoma samples than in the adjacent normal tissues. Linc00152 expression levels tightly correlated with lymph node metastasis station, remote metastasis and TNM staging. The Kaplan-Meier analysis suggested that high Linc00152 expression caused significantly poorer OS and DFS rates, and a multivariate analysis revealed that Linc00152 was an independent risk factor for both DFS and OS. Overexpression of Linc00152 in lung cancer cells stimulated proliferation, tumor cell invasion and migration. Knockdown of Linc00152 inhibited cell growth and cell invasion and migration. Finally, Linc00152 knockdown inhibited lung tumor growth and tumor metastasis in nude mice models. Conclusions: Our study suggests that Linc00152 independently predicts poor prognosis and promotes tumor progression in lung adenocarcinoma. Linc00152 needs to be considered as a potential molecular target in future cancer pharmacology.