The AQP-3 water channel is a pivotal modulator of glycerol-induced chloride channel activation in nasopharyngeal carcinoma cells

Zhang, Haifeng; Deng, Zhiqin; Yang, Lili; Hai, Luo; Liu, Shan-Wen; Li, Yuan; Wei, Yan; Peng, Shuang; Zhu, Linyan; Wang, Liwei; Chen, Lixin

doi:10.1016/j.biocel.2016.01.009

Cited by 14 publications

(7 citation statements)

References 54 publications

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“…Aquaporin is a protein located on the membranes of cells that controls the ingress and egress of water [36]. Studies have demonstrated that AQP3 and AQP8 can promote the reabsorption of excess water in the intestine, reduce the water content of feces, and control diarrhea [37,38]. In the present study, we found that EEDAR-H significantly promoted the expression of AQP3 and AQP8 and so relieved diarrhea.…”

Section: Discussionsupporting

confidence: 58%

Deep-Fried Atractylodis Rhizoma Protects against Spleen Deficiency-Induced Diarrhea through Regulating Intestinal Inflammatory Response and Gut Microbiota

Shi

Xiong

et al. 2019

IJMS

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According to the theories of traditional Chinese medicine, spleen deficiency often leads to diarrhea, and deep-fried Atractylodis Rhizoma (DAR) is commonly used for the treatment. However, the association between spleen deficiency and diarrhea remains unclear. The present study aimed to investigate the therapeutic effect of DAR for the treatment of diarrhea caused by spleen deficiency and analyze the related mechanisms. It was found that a high dose group of an ethanolic extract of deep-fried Atractylodis Rhizoma (EEDAR-H) significantly inhibited weight loss, diarrhea, and pathological changes in colon tissue induced by rhubarb. EEDAR-H was found to significantly reduce the level of intestinal inflammatory cytokines and increase the expression of gastrointestinal motility hormones. In addition, EEDAR-H significantly increased the expression of aquaporin 3 (AQP3) and aquaporin 8 (AQP8) and restored abnormal water metabolism; Shen-Ling-Bai-Zhu-San (SLBZS) induced the same effect as EEDAR-H. Additional tests on the mechanism found that EEDAR-H and SLBZS promoted the integrity of the intestinal barrier. Both significantly increased the expression of the tight junction protein ZO-1 and Occludin, inhibited the phosphorylation of p38MAPK and MLC, and significantly reduced the expression levels of PAR-2. Analysis of the gut microbiota indicated that overall changes in its structure were reversed after treatment with EEDAR-H or SLBZS, in addition to significant modulation of the abundance of different phyla. At the genus level, EEDAR-H or SLBZS significantly reduced the levels of potential pathogens and increased those of beneficial bacteria.

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Section: Discussionsupporting

confidence: 58%

Deep-Fried Atractylodis Rhizoma Protects against Spleen Deficiency-Induced Diarrhea through Regulating Intestinal Inflammatory Response and Gut Microbiota

Shi

Xiong

et al. 2019

IJMS

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“…Loss of ClC-7 leads to osteoporosis (2,14). Cl Ϫ channels are involved in regulation of the cell cycle, proliferation, migration, and apoptosis, as well as cell volume regulation (16,18,19,22,29,30,(35)(36)(37)(38). Whether all these Cl Ϫ channels are involved in the estrogen regulation of bone formation remains to be clarified.…”

Section: Discussionmentioning

confidence: 99%

Estradiol activates chloride channels via estrogen receptor-α in the cell membranes of osteoblasts

Deng

Peng

Zheng

et al. 2017

American Journal of Physiology-Cell Physiology

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Estrogen plays important roles in regulation of bone formation. Cl channels in the ClC family are expressed in osteoblasts and are associated with bone physiology and pathology, but the relationship between Cl channels and estrogen is not clear. In this study the action of estrogen on Cl channels was investigated in the MC3T3-E1 osteoblast cell line. Our results show that 17β-estradiol could activate a current that reversed at a potential close to the Cl equilibrium potential, with a sequence of anion selectivity of I > Br > Cl > gluconate, and was inhibited by the Cl channel blockers 5-nitro-2-(3-phenylpropylamino)-benzoate and 4,4'-diisothiocyano-2,2'-stilbene disulfonic acid. Knockdown of ClC-3 Cl channel expression by a specific small interfering RNA to ClC-3 attenuated activation of the 17β-estradiol-induced Cl current. Extracellular application of membrane-impermeable 17β-estradiol-albumin conjugates activated a similar current. The estrogen-activated Cl current could be inhibited by the estrogen receptor (ER) antagonist fulvestrant (ICI 182780). The selective ERα agonist, but not ERβ agonist, activated a Cl current similar to that induced by 17β-estradiol. Silencing ERα expression prevented activation of estrogen-induced currents. Immunofluorescence and coimmunoprecipitation experiments demonstrated that ClC-3 Cl channels and ERα were colocalized and closely related in cells. Estrogen promoted translocation of ClC-3 and ERα to the cell membrane from the nucleus. In conclusion, our findings show that Cl channels can be activated by estrogen via ERα on the cell membrane and suggest that the ClC-3 Cl channel may be one of the targets of estrogen in the regulation of osteoblast activity.

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“…Given its importance in cancer cell proliferation, apoptosis, migration and/or invasion, and drug resistance, VARC has been considered to be a promising target for cancer diagnosis, prognosis and therapy ( 15 – 17 ). However, the biological functions of the LRRC8 family proteins remain poorly understood.…”

Section: Introductionmentioning

confidence: 99%

High expression of leucine‑rich repeat‑containing�8A is indicative of a worse outcome of colon cancer patients by enhancing cancer cell growth and metastasis

et al. 2018

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To survive, cells need to avoid excessive volume change that jeopardizes structural integrity and stability of the intracellular milieu. Searching for the molecular identity of volume-regulated anion channel (VRAC) has yielded multiple potential candidates, but none has been confirmed. Recently, it is reported that leucine-rich repeat-containing 8A (LRRC8A) is a main molecular determinant of VRAC current. The biological functions of LRRC8 family proteins are poorly understood, particularly in cancer. In the present study, we investigated LRRC8A in the most common cancers of the digestive system. LRRC8A proteins were found to be abundantly expressed in the esophagus, stomach, duodenum, colon, rectum, liver and pancreas. LRRC8A was elevated in 60% of colorectal cancer patient tissues, which was higher than that in patients with cancer of the esophagus, stomach, duodenum, liver and pancreas. Colon cancer patients with high- expressed LRRC8A had a survival time of 54.9±5.5 months, shorter than that of patients with low-expressed LRRC8A (77.1±3.7). Moreover, survival time (52.6±7.3 months) of patients with metastases in the lymph nodes was shorter than that of patients without positive lymph nodes (72.2±3.6); patients with positive lymph nodes and an elevated LRRC8A expression had the highest mortality rate (~80%). These rates were not observed in rectal cancer. After LRRC8A protein was knocked down in colon cancer HCT116 cells, VRAC currents, migration and tumorigenesis in nude mice were significantly inhibited. In conclusion, we propose that LRRC8A could be a novel prognostic biomarker for colon cancer patient survival, and that the elevated expression of LRRC8A may enhance cancer cell growth and metastasis, and worsen the outcome of patients.

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The AQP-3 water channel is a pivotal modulator of glycerol-induced chloride channel activation in nasopharyngeal carcinoma cells

Cited by 14 publications

References 54 publications

Deep-Fried Atractylodis Rhizoma Protects against Spleen Deficiency-Induced Diarrhea through Regulating Intestinal Inflammatory Response and Gut Microbiota

Deep-Fried Atractylodis Rhizoma Protects against Spleen Deficiency-Induced Diarrhea through Regulating Intestinal Inflammatory Response and Gut Microbiota

Estradiol activates chloride channels via estrogen receptor-α in the cell membranes of osteoblasts

High expression of leucine‑rich repeat‑containing�8A is indicative of a worse outcome of colon cancer patients by enhancing cancer cell growth and metastasis

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