TRPV4 induces apoptosis via p38 MAPK in human lung cancer cells

Zhao, Yanyan; Wang, Jiaying; Li, Xuehui

doi:10.1590/1414-431x2021e10867

Cited by 14 publications

(4 citation statements)

References 36 publications

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“…59 It has been widely reported that many key genes affecting lung cancer function through these two pathways. 60,61 In this study, changes in HBA and HBB affected the synthesis of p38 and JNK proteins, suggesting that they may also have a similar mechanism of action. which is a new starting point on searching for biomarkers.…”

Section: Discussionsupporting

confidence: 51%

“…JNK signaling pathway regulates lamellipodium formation and cell mobility, and plays a critical role in lung cancer invasiveness and metastasis 59 . It has been widely reported that many key genes affecting lung cancer function through these two pathways 60,61 . In this study, changes in HBA and HBB affected the synthesis of p38 and JNK proteins, suggesting that they may also have a similar mechanism of action.…”

Section: Discussionmentioning

confidence: 56%

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Role of hemoglobin alpha and hemoglobin beta in non‐small‐cell lung cancer based on bioinformatics analysis

Kang

Qiu

Wang

et al. 2022

Molecular Carcinogenesis

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The differentially expressed genes (DEGs) were identified and screened differentially in non‐small‐cell lung cancer (NSCLC) using information from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus databases, and the correlation of DEGs in protein interaction, function, and pathway enrichment were analyzed to search for new biomarkers and potential therapeutic targets for NSCLC. Protein–protein interaction network (PPI) analysis showed that CDK1 and GNGT1 were the most significantly upregulated hub nodes, while FPR2 was the most significantly downregulated. Gene Ontology enrichment analysis showed that upregulated DEGs were significantly enriched in protein heterodimerization activity and other functions, while downregulated DEGs were enriched in functions such as heparin‐binding. Kyoto Encyclopedia of Genes and Genomes pathway analysis showed that upregulation of DEGs were significantly associated with neuroactive ligand‐receptor interaction pathways, while downregulation of DEGs were significantly associated with malaria pathways. According to the analysis results, we identified hemoglobin alpha (HBA) and hemoglobin beta (HBB) as the genes of interest for further study. Through tissue level and cell level experiments, we found that the expressions of HBA and HBB in NSCLC tissues were significantly lower than those in paracancerous tissues, and downregulation of HBA and HBB could significantly affect the proliferation ability of NSCLC cells. In addition, we also found that changes in HBA and HBB may affect NSCLC cells through the p38/MAPK pathway and JNK pathway, and ultimately affect the occurrence and development of NSCLC.

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Section: Discussionsupporting

confidence: 51%

Section: Discussionmentioning

confidence: 56%

Role of hemoglobin alpha and hemoglobin beta in non‐small‐cell lung cancer based on bioinformatics analysis

Kang

Qiu

Wang

et al. 2022

Molecular Carcinogenesis

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“…Overexpression of TRPV4 in lung cancer cells promotes apoptosis by stimulating the p38 MAPK pathways [71]. In squamous cell carcinoma (SSC), oxidative stress induced apoptosis within 24 h of H 2 O 2 application.…”

Section: Apoptosis Induced By Modulation Of the Redox Trp Channelsmentioning

confidence: 99%

TRP Channels in Tumoral Processes Mediated by Oxidative Stress and Inflammation

Piciu,

Balas,

Badea

et al. 2023

Antioxidants

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The channels from the superfamily of transient receptor potential (TRP) activated by reactive oxygen species (ROS) can be defined as redox channels. Those with the best exposure of the cysteine residues and, hence, the most sensitive to oxidative stress are TRPC4, TRPC5, TRPV1, TRPV4, and TRPA1, while others, such as TRPC3, TRPM2, and TRPM7, are indirectly activated by ROS. Furthermore, activation by ROS has different effects on the tumorigenic process: some TRP channels may, upon activation, stimulate proliferation, apoptosis, or migration of cancer cells, while others inhibit these processes, depending on the cancer type, tumoral microenvironment, and, finally, on the methods used for evaluation. Therefore, using these polymodal proteins as therapeutic targets is still an unmet need, despite their draggability and modulation by simple and mostly unharmful compounds. This review intended to create some cellular models of the interaction between oxidative stress, TRP channels, and inflammation. Although somewhat crosstalk between the three actors was rather theoretical, we intended to gather the recently published data and proposed pathways of cancer inhibition using modulators of TRP proteins, hoping that the experimental data corroborated clinical information may finally bring the results from the bench to the bedside.

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“…The inhibition of p38 MAPK reduces TRPV4's effects on the cell proliferation, apoptosis, and migration of those cells. Collectively, this can imply that TRPV4 is a candidate target for human lung cancer therapy [239].…”

Section: Trpv4mentioning

confidence: 99%

TRP Channels in Cancer: Signaling Mechanisms and Translational Approaches

Marini,

Titiz,

Souza Monteiro de Araújo

et al. 2023

Biomolecules

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Ion channels play a crucial role in a wide range of biological processes, including cell cycle regulation and cancer progression. In particular, the transient receptor potential (TRP) family of channels has emerged as a promising therapeutic target due to its involvement in several stages of cancer development and dissemination. TRP channels are expressed in a large variety of cells and tissues, and by increasing cation intracellular concentration, they monitor mechanical, thermal, and chemical stimuli under physiological and pathological conditions. Some members of the TRP superfamily, namely vanilloid (TRPV), canonical (TRPC), melastatin (TRPM), and ankyrin (TRPA), have been investigated in different types of cancer, including breast, prostate, lung, and colorectal cancer. TRP channels are involved in processes such as cell proliferation, migration, invasion, angiogenesis, and drug resistance, all related to cancer progression. Some TRP channels have been mechanistically associated with the signaling of cancer pain. Understanding the cellular and molecular mechanisms by which TRP channels influence cancer provides new opportunities for the development of targeted therapeutic strategies. Selective inhibitors of TRP channels are under initial scrutiny in experimental animals as potential anti-cancer agents. In-depth knowledge of these channels and their regulatory mechanisms may lead to new therapeutic strategies for cancer treatment, providing new perspectives for the development of effective targeted therapies.

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TRPV4 induces apoptosis via p38 MAPK in human lung cancer cells

Cited by 14 publications

References 36 publications

Role of hemoglobin alpha and hemoglobin beta in non‐small‐cell lung cancer based on bioinformatics analysis

Role of hemoglobin alpha and hemoglobin beta in non‐small‐cell lung cancer based on bioinformatics analysis

TRP Channels in Tumoral Processes Mediated by Oxidative Stress and Inflammation

TRP Channels in Cancer: Signaling Mechanisms and Translational Approaches

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