Activation of ClC‐3 chloride channel by 17β‐estradiol relies on the estrogen receptor α expression in breast cancer

Yang, Haifeng; Ma, Lianshun; Wang, Yawei; Zuo, Wanhong; Li, Bingxue; Yang, Yaping; Chen, Ye‐Hui; Chen, Lixin; Wang, Liwei; Zhu, Linyan

doi:10.1002/jcp.25963

Cited by 26 publications

(27 citation statements)

References 34 publications

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“…ClC-3 has been found in the highly malignant human breast cancer cell lines MDA-MB-231 and MCF-7 [ 3 ]. However, it is unknown whether insulin-like growth factor 1 (IGF-1) affects the expression of ClC-3.…”

Section: Resultsmentioning

confidence: 99%

“…This would suggest that ClC-3 may regulate pERK1/2. Over the past decade, ClC-3 was found to be expressed in human breast cancer, cervical cancer, prostate cancer, nasopharyngeal cancer, osteosarcoma, leukemia, and malignant glioma [ 3 10 ]. Several groups have reported that ClC-3 may regulate tumor cell proliferation, apoptosis, autophagy, cell cycle, migration, and invasion.…”

Section: Discussionmentioning

confidence: 99%

“…Recent studies have demonstrated that chloride channel-3 (ClC-3) is expressed in breast cancer [ 3 ], cervical cancer [ 4 ], prostate cancer [ 5 ], nasopharyngeal cancer [ 6 ], osteosarcoma [ 7 ], leukemia [ 8 ], and glioma tumors [ 9 ], and its expression increases with tumor progression. The functions of ClC-3 are associated with the pathophysiology and progression of tumors.…”

Section: Introductionmentioning

confidence: 99%

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Knockdown of Chloride Channel-3 Inhibits Breast Cancer GrowthIn VitroandIn Vivo

et al. 2018

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PurposeChloride channel-3 (ClC-3) is a member of the chloride channel family and plays a critical role in a variety of cellular activities. The aim of the present study is to explore the molecular mechanisms underlying the antitumor effect of silencing ClC-3 in breast cancer.MethodsHuman breast cancer cell lines MDA-MB-231 and MCF-7 were used in the experiments. Messenger RNA and protein expression were examined by quantitative real-time polymerase chain reaction and western blot analysis. Cell proliferation was measured by the bromodeoxyuridine method, and the cell cycle was evaluated using fluorescence-activated cell sorting. Protein interaction in cells was analyzed by co-immunoprecipitation. Tumor tissues were stained with hematoxylin-eosin and tumor burden was measured using the Metamorph software.ResultsBreast cancer tissues collected from patients showed an increase in ClC-3 expression. Knockdown of ClC-3 inhibited the secretion of insulin-like growth factor (IGF)-1, cell proliferation, and G1/S transition in breast cancer cells. In the mouse xenograft model of human breast carcinoma, tumor growth was significantly slower in animals injected with ClC-3-deficient cells compared with the growth of normal human breast cancer cells. In addition, silencing of ClC-3 attenuated the expression of proliferating cell nuclear antigen, Ki-67, cyclin D1, and cyclin E, as well as the activation of extracellular signalregulated protein kinases (ERK) 1/2, both in vitro and in vivo.ConclusionTogether, our data suggest that upregulation of ClC-3 by IGF-1 contributes to cell proliferation and tumor growth in breast cancer, and ClC-3 deficiency suppresses cell proliferation and tumor growth via the IGF/IGF receptor/ERK pathway.

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Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Knockdown of Chloride Channel-3 Inhibits Breast Cancer GrowthIn VitroandIn Vivo

et al. 2018

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“…Chloride channels participate in different processes of neoplastic transformation, including cell proliferation, migration, invasion, and metastasis (Peretti et al, 2015). Evidence provided by Yang et al (2018) suggests that the expression of the voltage-gated chloride channel CLC-3 is regulated by 17-b estradiol in breast cancer cells. MCF-7 cells treated with 17-b estradiol showed increased chloride currents that were blocked by 5-nitro-2-(3phenylpropil-amino) benzoic acid (NPPB), and 4-4d…”

Section: Chloride Channelsmentioning

confidence: 99%

Ion Channel Regulation by Sex Steroid Hormones and Vitamin D in Cancer: A Potential Opportunity for Cancer Diagnosis and Therapy

2020

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Many ion channels are involved in tumor development, promoting cancer cell proliferation, migration, invasion, and survival. Accordingly, some of them have been suggested as tumor markers and novel targets for cancer therapy. Some sex steroid hormones (SSH), including estrogens and androgens, favor cancer progression. Meanwhile, other steroid hormones like vitamin D may have anticancer properties. SSH and vitamin D modulate the expression of a number of ion channels in cancer cells from hormone-sensitive tissues, including breast, ovary, prostate, and cervix. Moreover, rapid effects of SSH may be mediated by their direct action on membrane ion channels. Here, we reviewed the SSH and vitamin D regulation of ion channels involved in cancer, and analyzed the potential molecular pathways implicated. In addition, we described the potential clinical use of ion channels in cancer diagnosis and therapy, taking advantage of their regulation by SSH and vitamin D. Since SSH are considered risk factors for different types of cancer, and ion channels play important roles in tumor progression, the regulation of ion channels by SSH and vitamin D may represent a potential opportunity for early cancer diagnosis and therapeutic approaches in SSH and vitamin D sensitive tumors.

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“…ClC3 overexpression is observed in tissues and the TNBC cell line MDA-MB-231 [60,61] This indicates that ClC3 can promote the progression of TNBC by acting on the ERK1/2 signaling pathway [60]. Nevertheless, relative research on ClC3 in TNBC is still very limited, and extensive work is needed in the further.…”

Section: Chloride Channelmentioning

confidence: 99%

Pathological role of ion channels and transporters in the development and progression of triple-negative breast cancer

Cheng

et al. 2020

Cancer Cell Int

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Breast cancer is a common malignancy in women. Among breast cancer types, triple-negative breast cancer (TNBC) tends to affect younger women, is prone to axillary lymph node, lung, and bone metastases; and has a high recurrence rate. Due to a lack of classic biomarkers, the currently available treatments are surgery and chemotherapy; no targeted standard treatment options are available. Therefore, it is urgent to find a novel and effective therapeutic target. As alteration of ion channels and transporters in normal mammary cells may affect cell growth, resulting in the development and progression of TNBC, ion channels and transporters may be promising new therapeutic targets for TNBC. This review summarizes ion channels and transporters related to TNBC and may provide new tumor biomarkers and help in the development of novel targeted therapies.

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Activation of ClC‐3 chloride channel by 17β‐estradiol relies on the estrogen receptor α expression in breast cancer

Cited by 26 publications

References 34 publications

Knockdown of Chloride Channel-3 Inhibits Breast Cancer GrowthIn VitroandIn Vivo

Knockdown of Chloride Channel-3 Inhibits Breast Cancer GrowthIn VitroandIn Vivo

Ion Channel Regulation by Sex Steroid Hormones and Vitamin D in Cancer: A Potential Opportunity for Cancer Diagnosis and Therapy

Pathological role of ion channels and transporters in the development and progression of triple-negative breast cancer

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