Anoctamin5 regulates cell migration and invasion in thyroid cancer

Chang, Zhengyan; Cai, Chunmiao; Han, Dong; Gao, Yaohui; Li, Qianyu; Feng, Lijin; Zhang, Wei; Zheng, Jiayi; Jin, Junyang; Zhang, Huizhen; Wei, Qing

doi:10.3892/ijo.2017.4113

Cited by 26 publications

(25 citation statements)

References 37 publications

(31 reference statements)

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“…Further, the expression of several members of the anoctamin family, such as ANO1, ANO5, ANO7, and ANO9, is correlated with the development of malignant tumors. Expression of ANO5 is downregulated in thyroid cancer, and knockdown of ANO5 promotes cell migration and invasion via regulation of the JAK/STAT3 signaling pathway . However, the exact role of ANO5 in prostate cancer has yet to be determined.…”

Section: Discussionmentioning

confidence: 99%

“…Expression of ANO5 is downregulated in thyroid cancer, and knockdown of ANO5 promotes cell migration and invasion via regulation of the JAK/STAT3 signaling pathway. 25 However, the exact role of ANO5 in prostate cancer has yet to be determined. The position of rs4622263 overlaps with a GATA binding protein 1-bound region and is predicted to alter the regulatory motif transcription factor CP2-like 1, which has been implicated in maintenance of pluripotency and self-renewal in embryonic stem cells and cancers, 28,29 according to the experimental chromatin immunoprecipitation sequencing data in the HaploReg database.…”

Section: Discussionmentioning

confidence: 99%

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Genetic association analysis identifies a role for ANO5 in prostate cancer progression

Chen

Huang

et al. 2020

Cancer Medicine

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Anoctamins were originally identified as a family of calcium‐activated chloride channels, but recently their roles in the development of different types of malignancies were suggested. Here, we evaluated the associations between 211 common single‐nucleotide polymorphisms in 10 anoctamin genes with biochemical recurrence (BCR) after radical prostatectomy (RP) for localized prostate cancer. Four SNPs (ANO4 rs585335, ANO5 rs4622263, ANO7 rs62187431, and ANO10 rs118005571) remained significantly associated with BCR after multiple test correction (P < .05 and q = 0.232) and adjustment for known prognostic factors. Expression quantitative trait loci analysis found that ANO5 rs4622263 C and ANO10 rs118005571 C alleles were associated with decreased mRNA expression levels. Moreover, lower expression of ANO5 was correlated with more advanced tumors and poorer outcomes in two independent prostate cancer cohorts. Taken together, ANO5 rs4622263 was associated with BCR, and ANO5 gene expression was correlated with patient prognosis, suggesting a pivotal role for ANO5 in prostate cancer progression.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Genetic association analysis identifies a role for ANO5 in prostate cancer progression

Chen

Huang

et al. 2020

Cancer Medicine

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“…In contrast, no significant decrease in HER2 transcription by this treatment was noted in YMB‐1 cells (Figure C). Chang et al showed that inhibition of ANO5 activated the JAK/STAT3 signaling pathway in thyroid cancer cells. High ANO1 activity in YMB‐1 cells may prevent the constitutive JAK/STAT3 signaling pathway.…”

Section: Discussionmentioning

confidence: 99%

Transcriptional repression of human epidermal growth factor receptor 2 by ClC‐3 Cl⁻/H⁺ transporter inhibition in human breast cancer cells

et al. 2018

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Recent studies have indicated that the intracellular concentration of chloride ions (Cl−) regulates gene expression in several types of cells and that Cl− modulators positively or negatively regulate the PI3K/AKT/mammalian target of rapamycin (mTOR) and signal transducer and activator of transcription (STAT)3 signaling pathways. We previously reported that the Ca2+‐activated Cl− channel anoctamine (ANO)1 regulated human epidermal growth factor receptor 2 (HER2) transcription in breast cancer YMB‐1 cells. However, the mechanisms underlying ANO1‐regulated HER2 gene expression have not yet been elucidated. In the present study, we showed the involvement of intracellular organelle ClC‐3 Cl−/H+ transporter in HER2 transcription in breast cancer MDA‐MB‐453 cells. The siRNA‐mediated inhibition of ClC‐3, but not ANO1, markedly repressed HER2 transcription in MDA‐MB‐453 cells. Subsequently, treatments with the AKT inhibitor AZD 5363 and mTOR inhibitor everolimus significantly enhanced HER2 transcription in MDA‐MB‐453 cells, whereas that with the STAT3 inhibitor 5,15‐diphenylporphyrin (5,15‐DPP) inhibited it. AKT and mTOR inhibitors also significantly enhanced HER2 transcription in YMB‐1 cells. The siRNA‐mediated inhibition of ClC‐3 and ANO1 resulted in increased AKT phosphorylation and decreased STAT3 phosphorylation in MDA‐MB‐453 and YMB‐1 cells, respectively. The intracellular Cl− channel protein CLIC1 was expressed in both cells; however, its siRNA‐mediated inhibition did not elicit the transcriptional repression of HER2. Collectively, our results demonstrate that intracellular Cl− regulation by ANO1/ClC‐3 participates in HER2 transcription, mediating the PI3K/AKT/mTOR and/or STAT3 signaling pathway(s) in HER2‐positive breast cancer cells, and support the potential of ANO1/ClC‐3 blockers as therapeutic options for patients with resistance to anti‐HER2 therapies.

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“…TMEM91 encodes a protein belonging to the transmembrane protein family which mediates a number of human physiological processes, such as the regulation of cell migration and invasion, constructs ion channels, and participates in the immune response [ 29 – 31 ]. At present, research on the TMEM family members focuses mostly on the field of cancer; however, their relationship with thyroid disease is unknown [ 32 ].…”

Section: Discussionmentioning

confidence: 99%

Copy Number Variation of Immune-Related Genes and Their Association with Iodine in Adults with Autoimmune Thyroid Diseases

Jin

Guan

Shen

et al. 2018

International Journal of Endocrinology

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Background Autoimmune thyroid diseases (AITD) are complex conditions that are caused by an interaction between genetic susceptibility and environmental triggers. Iodine is already known to be an environmental trigger for AITD, but genes associated with susceptibility need to be further assessed. Therefore, the aims of this study were to assess the association between copy number variations (CNVs) and AITD, to identify genes related with susceptibility to AITD, and to investigate the interaction between iodine status and CNVs in the occurrence of AITD. Methods Blood samples from 15 patients with AITD and 15 controls were assessed by chromosome microarray to identify candidate genes. The copy number of candidate genes and urinary iodine level was determined in adults from areas of different iodine statuses including 158 patients and 181 controls. Results The immune-related genes, SIRPB1 and TMEM91, were selected as candidate genes. The distribution of SIRPB1 CNV in AITD patients and controls was significantly different and was considered a risk factor for AITD. There was no significant association between urinary iodine level and candidate gene CNVs. Conclusion SIRPB1 CNV and an excess of iodine were risk factors for AITD, but an association with the occurrence of AITD was not found.

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Anoctamin5 regulates cell migration and invasion in thyroid cancer

Cited by 26 publications

References 37 publications

Genetic association analysis identifies a role for ANO5 in prostate cancer progression

Genetic association analysis identifies a role for ANO5 in prostate cancer progression

Transcriptional repression of human epidermal growth factor receptor 2 by ClC‐3 Cl⁻/H⁺ transporter inhibition in human breast cancer cells

Copy Number Variation of Immune-Related Genes and Their Association with Iodine in Adults with Autoimmune Thyroid Diseases

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Anoctamin5 regulates cell migration and invasion in thyroid cancer

Cited by 26 publications

References 37 publications

Genetic association analysis identifies a role for ANO5 in prostate cancer progression

Genetic association analysis identifies a role for ANO5 in prostate cancer progression

Transcriptional repression of human epidermal growth factor receptor 2 by ClC‐3 Cl−/H+ transporter inhibition in human breast cancer cells

Copy Number Variation of Immune-Related Genes and Their Association with Iodine in Adults with Autoimmune Thyroid Diseases

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Transcriptional repression of human epidermal growth factor receptor 2 by ClC‐3 Cl⁻/H⁺ transporter inhibition in human breast cancer cells