Reduced KLF4 is associated with lung cancer cell invasion by suppression of SPARC expression

Data indicat that the SPARC overexpression may play an important role in the initiation and development of non-small cell lung cancer (NSCLC), whereas KLF4 inhibits this process.

p53, KLF4, and p21 showed altered expression patterns in pulmonary neuroendocrine neoplasms. Lack of KLF4 and p21 expression was associated with accumulation of aggressive features in typical carcinoids.

KLF4 is probably repressed by histone acetylation in lung cancer.

Data suggest that the Kruppel-like factor 4 (KLF4) /telomerase reverse transcriptase (hTERT)/MAPK pathway is a potential new therapeutic target for lung cancer.

KLF4 inhibits the ability of invasion and the escape from response to chemotherapy by repressing the EMT process, and overexpression of KLF4 may be a potential strategy for lung cancer treatment, especially for cisplatin-resistant cases.

Kruppel-like factor 4 overexpression inhibited transforming growth factor-beta1, extracellular signal-regulated protein kinase, C-jun N-terminal kinase, and nuclear factor-kappaB expression levels in non-small cell lung cancer cells.

Knockdown of KLF4 promoted the migration and invasion of nonsmallcell lung cancer (NSCLC) cells, whereas rescue of KLF4 expression reduced cell motion ability in miR25overexpressing NSCLC cells.

Data show that Kruppel like factor 4 (KLF4) was overexpressed in met proto-oncogene protein (c-Met)-overexpressing non-small-cell lung cancer (NSCLC) cells and tissues.

Overexpression of KLF4 significantly reversed the effects of miR31205p on nonsmall cell lung cancer (NSCLC) cell proliferation and invasion. In conclusion, the present study demonstrated that miR31205p promoted NSCLC progression by directly targeting KLF4.

Overexpression of the long noncoding RNA TRHDE-AS1 inhibits the progression of lung cancer via the miRNA-103/KLF4 axis.