Recurrent activations of transient receptor potential vanilloid‐1 and vanilloid‐4 promote cellular proliferation and migration in esophageal squamous cell carcinoma cells

Huang, Rongqi; Wang, Fei; Yang, Yuchen; Ma, Wenbo; Lin, Zuoxian; Cheng, Na; Long, Yan; Deng, Simin; Li, Zhiyuan

doi:10.1002/2211-5463.12570

Cited by 36 publications

(29 citation statements)

References 63 publications

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“…Furthermore, TRPV1 and TRPV4 are functional in these cells, as shown with calcium imaging and whole cell patch clamp techniques. Finally, the overactivation of both channels leads to increased proliferation and migration of ESCC cells [75].…”

Section: Trpv2mentioning

confidence: 99%

TRP Channels in Digestive Tract Cancers

Stokłosa

Borgström

Kappel

et al. 2020

IJMS

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Cancers of the digestive tract are among the most prevalent types of cancer. These types of cancers are often diagnosed at a late stage, which results in a poor prognosis. Currently, many biomedical studies focus on the role of ion channels, in particular transient receptor potential (TRP) channels, in cancer pathophysiology. TRP channels show mostly non-selective permeability to monovalent and divalent cations. TRP channels are often dysregulated in digestive tract cancers, which can result in alterations of cancer hallmark functions, such as enhanced proliferation, migration, invasion and the inability to induce apoptosis. Therefore, TRP channels could serve as potential diagnostic biomarkers. Moreover, TRP channels are mostly expressed on the cell surface and ion channel targeting drugs do not need to enter the cell, making them attractive candidate drug targets. In this review, we summarize the current knowledge about TRP channels in connection to digestive tract cancers (oral cancer, esophageal cancer, liver cancer, pancreatic cancer, gastric cancer and colorectal cancer) and give an outlook on the potential of TRP channels as cancer biomarkers or therapeutic targets.

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Section: Trpv2mentioning

confidence: 99%

TRP Channels in Digestive Tract Cancers

Stokłosa

Borgström

Kappel

et al. 2020

IJMS

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“…Cells were cultured in 3 cm-diameter glass-bottom dishes for 24 h, thereafter medium was discarded and dishes were washed using 4°C Hank's balanced salt solution (HBSS), then cells were pre-incubated with 5 μM Fura-2-AM (Dojindo Laboratories) in 1 ml HBSS in the dishes for 45 min at 37°C in dark. Subsequently, the pre-incubated solution was pipetted away and cells were washed three times with HBSS to eliminate the extracellular Fura-2AM, then 1ml of HBSS was added and cells were incubated at 37°C in dark for 20 min for the full de-esteri cation of intracellular Fura-2AM, then calcium imaging was performed as we described previously [20].…”

Section: Intracellular Calcium Imagingmentioning

confidence: 99%

“…Protein extraction from cell lines and patient tissues and western blotting was performed as previously described [20,21]. Primary antibodies including rabbit anti-human TRPV2 (#sc-30155, Santa Cruz), rabbit anti-human β-Actin (#5125, CST), rabbit anti-human HIF1 (#A11945, Abclonal), rabbit anti-human TNFα (#A0277, Abclonal), rabbit anti-human NFkB (#A11163, Abclonal), rabbit anti-human HSP27 (#A0240, Abclonal), rabbit anti-human HSP40 (#A5504, Abclonal), rabbit anti-human HSP60 (#A0969, Abclonal), rabbit anti-human HSP70 (#A0284, Abclonal), rabbit anti-human HSP90 (#A1087, Abclonal), rabbit antihuman Calmodulin (#abs133163, Absin), rabbit anti-human PTEN (#abs134055, Absin), rabbit antihuman AKT1 (#sc-5298, Santa Cruz), rabbit anti-human PI3K (#A0265, Abclonal), rabbit anti-human PDK1 (#abs131621, Absin) and rabbit anti-human mTORC1 (#sc-517464, Santa Cruz) were applied according to manufacturer's instructions.…”

Section: Protein Extraction and Western Blottingmentioning

confidence: 99%

“…The cells were processed before being subjected to immuno uorescence analysis as described previously [20]. Rabbit anti-human TRPV2 primary antibody (#sc-30155, Santa Cruz) and Alexa Fluor 594 goat antirabbit secondary antibody (#ab-150080, Abcam) were used according to the manufacturers' instructions.…”

Section: Immuno Uorescence Analysis and Microscopymentioning

confidence: 99%

“…Cells were pretreated with the indicated dose of TRPV2 activator and/or inhibitors (dissolved and remained in culture medium until next medium renewal, medium was replaced twice per day) or exposed to heat (54°C) stimulation (water bath, thrice per day, 30 seconds per time) or heat (54°C) stimulation and/or tranilast (120 μM), VS5584 (95 nM) or oroxin B (156 nM ) respectively for up to 14 days. Heat stimulation was performed as described previously [20].…”

Section: Drug Administration and Thermal Stimulation Protocolmentioning

confidence: 99%

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Thermal stress involved in TRPV2 promotes tumorigenesis through the pathway of PI3K/Akt/mTOR in esophageal squamous cell carcinoma

Huang¹,

Li²,

Tian³

et al. 2020

Preprint

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BackgroundEsophageal squamous cell carcinoma (ESCC) is a leading cause of cancer death worldwide. Although the exposure of esophageal mucosa to heat stimuli has long been recognized as an important risk for the initiation and development of ESCC, its underlying mechanisms remain uncharacterized. MethodsWestern blotting and immunofluorescence were used to detect the expression and localization of transient receptor potential vanilloid receptor 2 (TRPV2) in the ESCC cells. The cancerous behaviors of the ESCC cells were evaluated by a single-cell culturing assay, a wound healing assay, a 3D culturing assay and a tube formation assay respectively. In vivo tumorigenicity and metastasis of the ESCC cells were examined via xenograft nude mouse models. Western blotting and IHC were performed to determine the expression profiles of TRPV2 in the ESCC patient tissues. TRPV2 knocked-out ESCC cell line was established using CRISPR-Cas9 gene editing technique.ResultsHere, we found that the expression of TRPV2, one of the thermally sensitive TRP family members, was upregulated in both ESCC cells and clinical samples. We further showed that activation of TRPV2 by recurrent acute thermal stress (54°C, a temperature unexpectedly much lower than those in many dietary modalities) or O1821 (20 μM), a TRPV2 agonist, promoted cancerous behaviors in ESCC cells. The proangiogenic capacity of the heat-challenged ESCC cells was also found to be enhanced profoundly in the tube formation assay; both tumor formation and metastasis that originated from the cells were substantially promoted in nude mouse models upon the activation of TRPV2. These effects were inhibited significantly by tranilast (120 μM), a TRPV2 inhibitor, and abolished by TRPV2 knock-out using CRISPR-Cas9 gene editing. Conversely, overexpression of TRPV2 by transfection of TRPV2 DNA into NE2 cells, could switch the cells to tumorigenesis upon activation of TRPV2. Mechanistically, the driving role of TRPV2 in the progression of ESCC is mainly regulated by the PI3K/Akt/mTOR signaling pathway. Application of a pan-PI3K/mTOR inhibitor and/or a PTEN activator resulted in markedly reduced ESCC cell proliferation. ConclusionsOur study first proved that TRPV2 plays an important role in the tumorigenesis of ESCC upon thermal stress. We revealed that TRPV2-PI3K/Akt/mTOR is a novel and promising target for the prevention and treatment of ESCC.

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Capsaicin: A chili pepper bioactive phytocompound with a potential role in suppressing cancer development and progression

Mondal,

Banerjee,

Terang

et al. 2024

Phytotherapy Research

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Cancer profoundly influences morbidity and fatality rates worldwide. Patients often have dismal prognoses despite recent improvements in cancer therapy regimens. However, potent biomolecules derived from natural sources, including medicinal and dietary plants, contain biological and pharmacological properties to prevent and treat various human malignancies. Capsaicin is a bioactive phytocompound present in red hot chili peppers. Capsaicin has demonstrated many biological effects, including antioxidant, anti‐inflammatory, antimicrobial, and anticarcinogenic capabilities. This review highlights the cellular and molecular pathways through which capsaicin exhibits antineoplastic activities. Our work also depicts the synergistic anticancer properties of capsaicin in conjunction with other natural bioactive components and approved anticancer drugs. Capsaicin inhibits proliferation in various cancerous cells, and its antineoplastic actions in numerous in vitro and in vivo carcinoma models impact oncogenesis, tumor‐promoting and suppressor genes, and associated signaling pathways. Capsaicin alone or combined with other phytocompounds or approved antineoplastic drugs triggers cell cycle progression arrest, generating reactive oxygen species and disrupting mitochondrial membrane integrity, ultimately stimulating caspases and promoting death. Furthermore, capsaicin alone or in combination can promote apoptosis in carcinoma cells by enhancing the p53 and c‐Myc gene expressions. In conclusion, capsaicin alone or in combination can have enormous potential for cancer prevention and intervention, but further high‐quality studies are needed to firmly establish the clinical efficacy of this phytocompound.

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Recurrent activations of transient receptor potential vanilloid‐1 and vanilloid‐4 promote cellular proliferation and migration in esophageal squamous cell carcinoma cells

Cited by 36 publications

References 63 publications

TRP Channels in Digestive Tract Cancers

TRP Channels in Digestive Tract Cancers

Thermal stress involved in TRPV2 promotes tumorigenesis through the pathway of PI3K/Akt/mTOR in esophageal squamous cell carcinoma

Capsaicin: A chili pepper bioactive phytocompound with a potential role in suppressing cancer development and progression

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