CXCR4/MIF axis amplifies tumor growth and epithelial-mesenchymal interaction in non-small cell lung cancer.
In conclusion, our data highlight the role of the CXCR4-OE/MIF/IL-6 axis in epithelial mesenchymal crosstalk and NSCLC progression. PMID: 32428553 [PubMed - as supplied by publisher]
In conclusion, CTC EMT is significantly related to Ki67 expression, and is a risk factor of NSCLC. PMID: 32655819 [PubMed]
Datta Epidemiologic studies have shown that vast majority of lung cancers (85–90%) are causally linked to tobacco smoking. Although much information has been gained about the effects of smoking on various signaling pathways, little is known about how deregulation of miRNAs leads to activation of oncogenes and inhibition of tumor suppressor genes in non-small cell lung cancer (NSCLC). Our previous study showed that smoking inhibits TGF-β-induced tumor suppressor functions through downregulation of Smad3 in lung cancer cells. In order to understand the upstream mechanism of downregulation of Smad3 by s...
AA Abstract Resistance to chemotherapeutic drugs is a critical problem in cancer therapy, but the underlying mechanism has not been fully elucidated. TP53-induced glycolysis regulatory phosphatase (TIGAR), an important glycolysis and apoptosis regulator, plays a crucial role in cancer cell survival by protecting cells against oxidative stress-induced apoptosis. In the present study, we investigated whether TIGAR is involved in epithelial-mesenchymal transition (EMT) in doxorubicin (DOX)-resistant human non-small cell lung cancer (NSCLC), A549/DOX cells. We found that the expression of TIGAR was s...
Conclusion: NudCD1 promotes the proliferation and metastasis of NSCLC cells via activation of IGF1R-ERK1/2, which indicates that NudCD1 may be a potential therapy target of NSCLC.Pathobiology
Conclusion: The fluid-assisted separation technology disc platform enables serial monitoring of CTC counts, DNA mutations, as well as unbiased molecular characterization of individual CTCs associated with tumor progression during targeted therapy.
Conclusion: Our results showed that the effect of EphB1 on the migration and invasion was context-specific and was dependent on EphB1 phosphorylation.
CONCLUSION: c-Met kinase inhibitors have emerged as exciting new drug classes in the treatment of all kinds of cancers, especially the Non-Small Cell Lung Cancer (NSCLC) with tumor resistance. More attention should be paid on the natural product to find novel c-Met kinase inhibitors. PMID: 32603284 [PubMed - as supplied by publisher]
We describe the adaptive and innate components involved in the EOC immune response, including infiltrating tumor-specific T lymphocytes, B lymphocytes, and natural killer and myeloid cells. In addition, we highlight the rationale behind the use of EOC preclinical mouse models to assess resistance to immunotherapy, and we summarize the main preclinical studies that yielded anti-EOC immunotherapeutic strategies. Finally, we focus on major published or ongoing immunotherapy clinical trials concerning EOC.
Epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs) rechallenged therapy for EGFR-mutant NSCLC patients who acquired resistance showed moderate efficacy[1,2]. Nevertheless, the majority of NSCLC patients gradually acquire resistance over 6-18.9 months of therapy. Notably, approximately 30% of NSCLC patients with EGFR mutations develop primary resistance EGFR-TKIs[3 –5]. Hence, it is of great importance to explore the exact mechanism of EGFR-TKIs resistance, along with identification of solutions to battle the resistance.