Transient Receptor Potential Type Vanilloid 1 Suppresses Skin Carcinogenesis

Bode, Ann M.; Cho, Yong‐Yeon; Zheng, Duo; Zhu, Feng; Ericson, Marna E.; Ya, Wei; Yao, Ke; Dong, Zigang

doi:10.1158/0008-5472.can-08-3263

Cited by 93 publications

(72 citation statements)

References 42 publications

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“…A recent report by The Cancer Genome Atlas (TCGA) Network identified abundant somatic mutations in genes encoding calpains (CAPN1-CAPN13), PTP1B (PTPN1), TRPV1, and other TRP channels, demonstrating their importance in the pathogenesis of CRC (73). TRPV1 has been previously associated with regulation of EGFR signaling in the context of skin carcinogenesis (74). Our data differ from these findings in that we did not find any evidence for TRPV1-mediated EGFR degradation in IECs.…”

Section: (H) Apccontrasting

confidence: 99%

Ion channel TRPV1-dependent activation of PTP1B suppresses EGFR-associated intestinal tumorigenesis

Jong¹,

Takahashi²,

Harris³

et al. 2014

J. Clin. Invest.

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Section: (H) Apccontrasting

confidence: 99%

Ion channel TRPV1-dependent activation of PTP1B suppresses EGFR-associated intestinal tumorigenesis

Jong¹,

Takahashi²,

Harris³

et al. 2014

J. Clin. Invest.

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“…Kim et al (1999) suggested that capsaicin uptake in the diet could play a role in inhibition of tumorigenesis induced by MNNG. Bode et al (2009) reported a striking increase in skin carcinogenesis in TRPV1 knock-out (TRPV1 -/-) mice in a two-stage carcinogenesis experiment. When TRPV1 -/-mice were initiated with DMBA and then promoted with TPA over 21 weeks, a significant enhancement of tumor development relative to wild-type controls was found.…”

Section: Teel and Huynh 1999mentioning

confidence: 99%

A Comprehensive Review of the Carcinogenic and Anticarcinogenic Potential of Capsaicin

et al. 2012

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Human exposure to capsaicin, the most abundant pungent chili pepper component, is ubiquitous. Evaluation of capsaicin's carcinogenic potential has produced variable results in in vitro and in vivo genotoxicity and carcinogenicity assays. The capsaicin tested in older studies was often from pepper plant extracts and included other capsaicinoids and diverse impurities. Recent studies utilizing high-purity capsaicin and standardized protocols provide evidence that the genotoxic and carcinogenic potential of capsaicin is quite low and that the purity of capsaicin is important. Several small epidemiological studies suggest a link between capsaicin consumption and stomach or gall bladder cancer, but contamination of capsaicin-containing foods with known carcinogens renders their interpretation problematic. The postulated ability of capsaicin metabolites to damage DNA and promote carcinogenesis remains unsupported. Anticancer activities of capsaicin have been widely reported, as it inhibits the activity of carcinogens and induces apoptosis in numerous cancer cell lines in vitro and explanted into rodents. Diverse mechanisms have been postulated for capsaicin's anticancer properties. One hypothesis is that inhibition of cytochrome P450 enzymes-particularly CYP2E1-retards carcinogen activation but is contradicted by the low potency of capsaicin for CYP inhibition. The potential for dietary capsaicin to act as a chemopreventative is now widely postulated.

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“…Altered calcium signaling through such changes in expression may contribute to tumorigenesis via calciumsensitive pathways such as apoptosis, migration, and proliferation (2)(3)(4). Examples of calcium channels contributing to altered calcium signaling in cancer cells include the store-operated calcium channel ORAI1 and many members of the transient receptor potential (TRP) channel family (5)(6)(7)(8)(9)(10).…”

Section: Introductionmentioning

confidence: 99%

Calcium Channel TRPV6 as a Potential Therapeutic Target in Estrogen Receptor–Negative Breast Cancer

Peters

Simpson

Bassett

et al. 2012

Molecular Cancer Therapeutics

112

106

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Calcium signaling is a critical regulator of cell proliferation. Elevated expression of calcium channels and pumps is a characteristic of some cancers, including breast cancer. We show that the plasma membrane calcium channel TRPV6, which is highly selective for Ca 2þ , is overexpressed in some breast cancer cell lines. Silencing of TRPV6 expression in a breast cancer cell line with increased endogenous TRPV6 expression leads to a reduction in basal calcium influx and cellular proliferation associated with a reduction in DNA synthesis. TRPV6 gene amplification was identified as one mechanism of TRPV6 overexpression in a subset of breast cancer cell lines and breast tumor samples. Analysis of two independent microarray expression datasets from breast tumor samples showed that increased TRPV6 expression is a feature of estrogen receptor (ER)-negative breast tumors encompassing the basal-like molecular subtype, as well as HER2-positive tumors. Breast cancer patients with high TRPV6 levels had decreased survival compared with patients with low or intermediate TRPV6 expression. Our findings suggest that inhibitors of TRPV6 may offer a novel therapeutic strategy for the treatment of ER-negative breast cancers. Mol Cancer Ther; 11(10); 2158-68. Ó2012 AACR.

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Transient Receptor Potential Type Vanilloid 1 Suppresses Skin Carcinogenesis

Cited by 93 publications

References 42 publications

Ion channel TRPV1-dependent activation of PTP1B suppresses EGFR-associated intestinal tumorigenesis

Ion channel TRPV1-dependent activation of PTP1B suppresses EGFR-associated intestinal tumorigenesis

A Comprehensive Review of the Carcinogenic and Anticarcinogenic Potential of Capsaicin

Calcium Channel TRPV6 as a Potential Therapeutic Target in Estrogen Receptor–Negative Breast Cancer

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