ArticleMolecular cancer2013
TMEM16A alternative splicing coordination in breast cancer.
Article in Molecular cancer, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 39 citations in OpenAlex.
- Carrier-free procyanidin-ferric nanonetworks loading gefitinib to inhibit TMEM16A-EGFR mutual activation loop for photothermally enhanced breast cancer targeted therapy.Materials today. Bio · 2025Article
- High level of ANO1 promotes pancreatic cancer growth in concert with oncogenic KRAS.Molecular biology reports · 2023Article
- Pathophysiological role of ion channels and transporters in HER2-positive breast cancer.Cancer gene therapy · 2022Review
- Role of ANO1 in tumors and tumor immunity.Journal of cancer research and clinical oncology · 2022Review
- Chloride Channels and Transporters: Roles beyond Classical Cellular Homeostatic pH or Ion Balance in Cancers.Cancers · 2022Review
- The multifaceted role of TMEM16A in cancer.Cell calcium · 2019Review
- Direct repression of anoctamin 1 (FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019Article
- Review
- Identification of candidate target genes for endometrial cancer, such as ANO1, using weighted gene co-expression network analysis.Experimental and therapeutic medicine · 2019Article
- Anoctamin Channels in Human Myometrium: A Novel Target for Tocolysis.Reproductive sciences (Thousand Oaks, Calif.) · 2018Article
- CaThe Journal of biological chemistry · 2018Article
- Chloride Homeostasis in Neurons With Special Emphasis on the Olivocerebellar System: Differential Roles for Transporters and Channels.Frontiers in cellular neuroscience · 2018Review
- Cell-specific regulation of proliferation by Ano1/TMEM16A in breast cancer with different ER, PR, and HER2 status.Oncotarget · 2017Article
- Isoform Evolution in Primates through Independent Combination of Alternative RNA Processing Events.Molecular biology and evolution · 2017Article
- Cell-specific mechanisms of TMEM16A CaMolecular cancer · 2017Review
- Inhibition of calcium-activated chloride channel ANO1 suppresses proliferation and induces apoptosis of epithelium originated cancer cells.Oncotarget · 2016Article
- A novel exon in the human Ca2+-activated Cl- channel Ano1 imparts greater sensitivity to intracellular Ca2.American journal of physiology. Gastrointestinal and liver physiology · 2015Article
- Molecular and functional significance of Ca(2+)-activated Cl(-) channels in pulmonary arterial smooth muscle.Pulmonary circulation · 2015Review
- TMEM16 proteins: unknown structure and confusing functions.Journal of molecular biology · 2015Review
- Inhibition of Calcium-Activated Chloride Channel ANO1/TMEM16A Suppresses Tumor Growth and Invasion in Human Lung Cancer.PloS one · 2015Article
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundTMEM16A, also known as Anoctamin-1, is a calcium-activated chloride channel gene overexpressed in many tumors. The role of TMEM16A in cancer is not completely understood and no data are available regarding the potential tumorigenic properties of the multiple isoforms generated by alternative splicing (AS).
methodsWe evaluated TMEM16A AS pattern, isoforms distribution and Splicing Coordination (SC), in normal tissues and breast cancers, through a semi-quantitative PCR-assay that amplifies transcripts across three AS exons, 6b, 13 and 15.
resultsIn breast cancer, we did not observe an association either to AS of individual exons or to specific TMEM16A isoforms, and induced expression of the most common isoforms present in tumors in the HEK293 Flp-In Tet-ON system had no effect on cellular proliferation and migration. The analysis of splicing coordination, a mechanism that regulates AS of distant exons, showed a preferential association of exon 6b and 15 in several normal tissues and tumors: isoforms that predominantly include exon 6b tend to exclude exon 15 and vice versa. Interestingly, we found an increase in SC in breast tumors compared to matched normal tissues.
conclusionsAs the different TMEM16A isoforms do not affect proliferation or migration and do not associate with tumors, our results suggest that the resulting channel activities are not directly involved in cell growth and motility. Conversely, the observed increase in SC in breast tumors suggests that the maintenance of the regulatory mechanism that coordinates distant alternative spliced exons in multiple genes other than TMEM16A is necessary for cancer cell viability.
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