Let-7c overexpression

Overexpression of TAGLN reverses the promoting role of let-7c-5p on oral cancer cells. Our findings highlight the role of exosomal let-7c-5p in enhancing oral cancer cell aggressiveness by downregulating TAGLN expression, highlighting its potential as a diagnostic and therapeutic strategy.

Further mechanistic research revealed that the overexpression of Let-7c or miR-200c can reverse the malignant evolution of EOC cells induced by IL-6, including EMT, invasion, and metastasis. Consequently, our results suggest that IL-6 regulates the expression of Let-7c and miR-200c through the STAT3/HIF-1α pathway, thereby promoting EMT, invasion, and metastasis in EOC cells.

The findings suggest that let-7c-5p exerts an antitumor function by inhibiting the DUSP7-mediated MAPK-ERK pathway. Both DUSP7 and let-7c-5p have the potential to serve as prognostic biomarkers in CRC patients.

In summary, ANW inhibits the growth and metastasis of NSCLC cells in vivo and in vitro by upregulating the expression of let-7c-3p, which can regulate the PI3K/AKT/mTOR signaling pathway. PIK3CA is the main target of let-7c-3p.

The serum MicroRNA let-7c level was found to be an independent predictive biomarker in the FOLFIRINOX treatment group.

CuB regulated cell proliferation and apoptosis by inhibiting the XIST/miR-let-7c/IL-6/STAT3 axis in lung cancer. These findings indicate CuB may have the possibility of clinical application in lung cancer treatment.

Silencing AURKB or overexpressing let-7c-5p both could suppress proliferation, migration, and invasion and stimulate apoptosis, while overexpressing the two simultaneously could reverse such effect. Forced expression of let-7c-5p inhibited proliferation, migration, and invasion and accelerated apoptosis of LUAD cells by inhibiting AURKB, which may provide a new way to understand the malignant progression of LUAD.

Importantly, we found that LCSCs with knockdown of Lin28A or over-expression of let-7c exhibited inhibited carcinogenesis and disrupted expansion in vivo. Our study uncovered the functions and mechanisms of the Lin28A/let-7c/MAPK signaling pathway in promoting the proliferation and cancer stemness of LCSCs, which might be a potential therapeutic target for reducing and even eliminating LCSCs in the future.

RNAi knockdown of SOX13 reduced the invasion and colony formation ability of pancreatic cancer cells. The identification of key miRNA-mRNA gene interactions and networks provide potential diagnostic and therapeutic strategies for better treatment options for pancreatic cancer patients.

Therefore, let-7c may be considered to be an anti-oncogene of LIHC. The present study may provide novel targets and strategies for the diagnosis and treatment of LIHC.

Our results suggest an important role of let-7c in regulating EMT and the resulting Osimertinib resistance in T790M NSCLCs. More clinical studies need to be performed to fully understand the translational relevance of this novel mechanism.