Keratin 80 Promotes Migration and Invasion of Non-Small Cell Lung Cancer Cells by Regulating the TGF-β/SMAD Pathway

Tong, Yueyang; Chen, Xueyuan; Feng, Zhijun; Xu, Changqing; Li, Yaqian

doi:10.1155/2022/2630351

Cited by 5 publications

(2 citation statements)

References 34 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Furthermore, KRT80 knockdown was reported to inhibit proliferation, anti-apoptosis, anti-pyroptosis, migration, invasion, and epithelial- mesenchymal transition (EMT) in gastric cancer cells. 10 Tong et al 14 found that depletion of KRT80 restrained proliferation, migration, invasion, and EMT of lung cancer cells by affecting the TGF-β/SMAD pathway. Liu et al 12 found that miR-206/ETS1-mediated KRT80 overexpression promoted the proliferation, the transition from G 1 phase to S phase, invasion, migration and EMT of ovarian cancer cells by MEK/ERK pathway.…”

Section: Discussionmentioning

confidence: 99%

The facilitating effects of KRT80 on chemoresistance, lipogenesis, and invasion of esophageal cancer

Yun,

Li,

Yin

et al. 2024

Cancer Biology & Therapy

View full text Add to dashboard Cite

Keratin 80 (KRT80) is a filament protein that makes up one of the major structural fibers of epithelial cells, and involved in cell differentiation and epithelial barrier integrity. Here, KRT80 mRNA expression was found to be higher in esophageal cancer than normal epithelium by RT-PCR and bioinformatics analysis ( p < .05), opposite to KRT80 methylation ( p < .05). There was a negative relationship between promoter methylation and expression level of KRT80 gene in esophageal cancer ( p < .05). KRT80 mRNA expression was positively correlated with the differentiation, infiltration of immune cells, and poor prognosis of esophageal cancer ( p < .05). KRT80 mRNA expression was positively linked to no infiltration of immune cells, the short survival time of esophageal cancers ( p < .05). The differential genes of KRT80 mRNA were involved in fat digestion and metabolism, peptidase inhibitor, and intermediate filament, desosome, keratinocyte differentiation, epidermis development, keratinization, ECM regulator, complement cascade, metabolism of vitamins and co-factor ( p < .05). KRT-80-related genes were classified into endocytosis, cell adhesion molecule binding, cadherin binding, cell–cell junction, cell leading edge, epidermal cell differentiation and development, T cell differentiation and receptor complex, plasma membrane receptor complex, external side of plasma membrane, metabolism of amino acids and catabolism of small molecules, and so forth ( p < .05). KRT80 knockdown suppressed anti-apoptosis, anti-pyroptosis, migration, invasion, chemoresistance, and lipogenesis in esophageal cancer cells ( p < .05), while ACC1 and ACLY overexpression reversed the inhibitory effects of KRT80 on lipogenesis and chemoresistance. These findings indicated that up-regulated expression of KRT80 might be involved in esophageal carcinogenesis and subsequent progression, aggravate aggressive phenotypes, and induced chemoresistance by lipid droplet assembly and ACC1- and ACLY-mediated lipogenesis.

show abstract

Section: Discussionmentioning

confidence: 99%

The facilitating effects of KRT80 on chemoresistance, lipogenesis, and invasion of esophageal cancer

Yun,

Li,

Yin

et al. 2024

Cancer Biology & Therapy

View full text Add to dashboard Cite

show abstract

“…The GO term ‘cell differentiation’ includes TBL1X/Y related 1 ( TBL1XR1 ), and in NSCLC cells, TBL1XR1 has been shown to promote cell survival, proliferation, and metastasis [ 64 ]. The GO term ‘cytosol’ includes Keratin 80, which is known to promote the migration and invasion of NSCLC cells by regulating the TGF-β/SMAD pathway [ 65 ]. The GO term ‘catalytic activity’ includes C-C motif chemokine ligand 5, which activates αvβ3 integrin to promote migration as facilitated by the PI3K/Akt pathway through the activations of IKKα/β and NF-κB pathways in NSCLC cells [ 66 ].…”

Section: Discussionmentioning

confidence: 99%

MALAT1-regulated gene expression profiling in lung cancer cell lines

Roh,

Kim,

et al. 2023

BMC Cancer

View full text Add to dashboard Cite

Background Non-small cell lung cancer (NSCLC) is the most common type of lung cancer and has a poor prognosis. Identifying biomarkers based on molecular mechanisms is critical for early diagnosis, timely treatment, and improved prognosis of lung cancer. MALAT1 has been reported to have overexpressed and tumor-promoting functions in NSCLC. It has been proposed as a potential biomarker for the diagnosis and prognosis of cancer. Therefore, this study was conducted to profile the changes in gene expression according to the regulation of expression of MALAT1 in NSCLC cell lines and to investigate the correlation through bioinformatic analysis of differentially expressed genes (DEGs). Methods MALAT1 expression levels were measured using RT-qPCR. The biological functions of MALAT1 in NSCLC were analyzed by cell counting, colony forming, wound-healing, and Transwell invasion assays. In addition, gene expression profiling in response to the knockdown of MALAT1 was analyzed by transcriptome sequencing, and differentially expressed genes regulated by MALAT1 were performed by GO and KEGG pathway enrichment analyses. Bioinformatic databases were used for gene expression analysis and overall survival analysis. Results Comparative analysis versus MALAT1 expression in MRC5 cells (a normal lung cell line) and the three NSCLC cell lines showed that MALAT1 expression was significantly higher in the NSCLC cells. MALAT1 knockdown decreased cell survival, proliferation, migration, and invasion in all three NSCLC cell lines. RNA-seq analysis of DEGs in NSCLC cells showed 198 DEGs were upregulated and 266 DEGs downregulated by MALAT1 knockdown in all three NSCLC cell lines. Survival analysis on these common DEGs performed using the OncoLnc database resulted in the selection of five DEGs, phosphoglycerate mutase 1 (PGAM1), phosphoglycerate mutase 4 (PGAM4), nucleolar protein 6 (NOL6), nucleosome assembly protein 1 like 5 (NAP1L5), and sestrin1 (SESN1). The gene expression levels of these selected DEGs were proved to gene expression analysis using the TNMplot database. Conclusion MALAT1 might function as an oncogene that enhances NSCLC cell survival, proliferation, colony formation, and invasion. RNA-seq and bioinformatic analyses resulted in the selection of five DEGs, PGAM1, PGAM4, NOL6, NAP1L5, and SESN1, which were found to be closely related to patient survival and tumorigenesis. We believe that further investigation of these five DEGs will provide valuable information on the oncogenic role of MALAT1 in NSCLC.

show abstract

KRT80 in hepatocellular carcinoma plays oncogenic role via epithelial–mesenchymal transition and PI3K/AKT pathway

Hua,

Yan,

et al. 2024

IUBMB Life

View full text Add to dashboard Cite

Hepatocellular carcinoma (HCC), a globally prevalent form of cancer, is featured by aggressive growth and early metastasis. Elucidating the underlying mechanism and identifying the effective therapy are critical for advanced HCC patients. In the study, we detect that KRT80 was upregulated in HCC samples. HCC patients with higher KRT80 are associated with worse overall survival after surgery. Gain‐of and loss‐of function studies show that KRT80 enhanced HCC cells proliferation, migration, invasion, and angiogenesis, whereas its silencing abolishes the effects in vivo and in vitro. Mechanistic investigation shows that KRT80 may function as an independent prognostic risk factor and act as an oncogene by influencing EMT and modulating the PI3K/AKT signaling pathway. Together, these findings suggest that KRT80 may be a potential oncogene and a good indicator in predicting prognosis. Targeting KRT80 can offer new insights into the prevention and treatment of HCC.

show abstract

Keratin 80 Promotes Migration and Invasion of Non-Small Cell Lung Cancer Cells by Regulating the TGF-β/SMAD Pathway

Cited by 5 publications

References 34 publications

The facilitating effects of KRT80 on chemoresistance, lipogenesis, and invasion of esophageal cancer

The facilitating effects of KRT80 on chemoresistance, lipogenesis, and invasion of esophageal cancer

MALAT1-regulated gene expression profiling in lung cancer cell lines

KRT80 in hepatocellular carcinoma plays oncogenic role via epithelial–mesenchymal transition and PI3K/AKT pathway

Contact Info

Product

Resources

About