Chemoresistance Mechanisms in Non-Small Cell Lung Cancer—Opportunities for Drug Repurposing

Kaur, Rajdeep; Suresh, P. K.

doi:10.1007/s12010-023-04595-7

Cited by 2 publications

(1 citation statement)

References 279 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Non-small cell lung cancer (NSCLC) and small cell lung cancer (SCLC) constitute the two primary forms of lung cancer ( 2 ). NSCLC accounts for 80–85% of all cases of lung cancer, establishing it as a predominant subtype within the spectrum of lung carcinomas ( 3 ). NSCLC is primarily caused by exposure to risk factors such as smoking, secondhand smoke, occupational carcinogens, and environmental pollutants, which can lead to the development of genetic mutations and cellular abnormalities in the lung ( 4 ).…”

Section: Introductionmentioning

confidence: 99%

Regulatory role of the miR-142-3p/CDC25C axis in modulating autophagy in non-small cell lung cancer

Meng,

Song,

Cong

et al. 2024

Transl Lung Cancer Res

View full text Add to dashboard Cite

Background With its diverse genetic foundation and heterogeneous nature, non-small cell lung cancer (NSCLC) needs a better comprehension of prognostic evaluation and efficient treatment targeting. Methods Bioinformatics analysis was performed of The Cancer Genome Atlas (TCGA)-NSCLC and GSE68571 dataset. Overlapping differentially expressed genes (DEGs) were used for functional enrichment analysis and constructing the protein-protein interaction (PPI) network. In addition, key prognostic genes were identified through prognostic risk models, and their expression levels were verified. The phenotypic effects of cell division cycle 25C ( CDC25C ) regulation on NSCLC cell lines were assessed by in vitro experiments using various techniques such as flow cytometry, Transwell, and colony formation. Protein levels related to autophagy and apoptosis were assessed, specifically examining the impact of autophagy inhibition [3-methyladenine (3-MA)] and the miR-142-3p/ CDC25C axis on this regulatory system. Results CDC25C was identified as a key prognostic marker in NSCLC, showing high expression in tumor samples. In vitro experiments showed that CDC25C knockdown markedly reduced the capacity of cells to proliferate, migrate, invade, trigger apoptosis, and initiate cell cycle arrest. CDC25C and miR-142-3p displayed a reciprocal regulatory relationship. CDC25C reversed the inhibitory impacts of miR-142-3p on NSCLC cell cycle proliferation and progression. The synergy of miR-142-3p inhibition, CDC25C silencing, and 3-MA treatment was shown to regulate NSCLC cell processes including proliferation, apoptosis, and autophagy. Conclusions MiR-142-3p emerged as a key player in governing autophagy and apoptosis by directly targeting CDC25C expression. This emphasizes the pivotal role of the miR-142-3p/ CDC25C axis as a critical regulatory pathway in NSCLC.

show abstract

Section: Introductionmentioning

confidence: 99%

Regulatory role of the miR-142-3p/CDC25C axis in modulating autophagy in non-small cell lung cancer

Meng,

Song,

Cong

et al. 2024

Transl Lung Cancer Res

View full text Add to dashboard Cite

show abstract

Carcinoma–Astrocyte Gap Junction Interruption by a Dual-Targeted Biomimetic Liposomal System to Attenuate Chemoresistance and Treat Brain Metastasis

Cheng,

Xu,

et al. 2024

ACS Nano

View full text Add to dashboard Cite

Brain metastasis contributes substantially to the morbidity and mortality of various malignancies and is characterized by high chemoresistance. Intracellular communication between carcinoma cells and astrocytes through gap junctions, which are assembled mainly by the connexin 43 protein, has been shown to play a vital role in this process. However, effectively blocking the gap junctions between the two cell types remains extremely challenging because of insufficient drug delivery to the target site. Herein, we designed a connexin blocker-carbenoxolone (CBX)-loaded biomimetic liposomal system with artificial liposomes fused with brain metastatic cell and reactive astrocyte membranes (LAsomes) to block gap junctions and attenuate chemoresistance. LAsomes effectively penetrated the blood−brain barrier via semaphorin 4D (SEMA 4D)�Plexin B1 interactions and actively migrated to their source cells via homotypic recognition. Consequently, LAsomes effectively inhibited material transfer and Ca 2+ flow from metastatic cells to astrocytes via gap junctions, thereby markedly increasing the sensitivity of metastatic tumor cells to chemotherapy. These results reveal that closing the gap junctions may be a promising therapeutic strategy for intractable brain metastasis.

show abstract

Chemoresistance Mechanisms in Non-Small Cell Lung Cancer—Opportunities for Drug Repurposing

Cited by 2 publications

References 279 publications

Regulatory role of the miR-142-3p/CDC25C axis in modulating autophagy in non-small cell lung cancer

Regulatory role of the miR-142-3p/CDC25C axis in modulating autophagy in non-small cell lung cancer

Carcinoma–Astrocyte Gap Junction Interruption by a Dual-Targeted Biomimetic Liposomal System to Attenuate Chemoresistance and Treat Brain Metastasis

Contact Info

Product

Resources

About