title: Anoctamin 6 regulates C2C12 myoblast proliferation.
abstract: Anoctamin 6 (Ano6) belongs to a conserved gene family (TMEM16) predicted to code for eight transmembrane proteins with putative Ca2+-activated chloride channel (CaCC) activity. Recent work revealed that disruption of ANO6 leads to a blood coagulation defect and impaired skeletal development. However, its function in skeletal muscle cells remains to be determined. By using a RNA interference mediated (RNAi) loss-of-function approach, we show that Ano6 regulates C2C12 myoblast proliferation. Ano6 is highly expressed in C2C12 myoblasts and its expression decreases upon differentiation. Knocking down Ano6 significantly reduces C2C12 myoblast proliferation but has minimal effect on differentiation. Ano6 deficiency significantly reduces ERK/AKT phosphorylation, which has been shown to be involved in regulation of cancer cell proliferation by another Anoctamin member. Taken together, our data demonstrate for the first time that Ano6 plays an essential role in C2C12 myoblast proliferation, likely via regulating the ERK/AKT signaling pathway.
authors.affiliation: Department of Cell and Molecular Physiology, Loyola University Chicago Health Science Division, Maywood, Illinois, United States of America.
authors.forename: Piming
authors.initials: P
authors.lastname: Zhao
authors.affiliation: Department of Cell and Molecular Physiology, Loyola University Chicago Health Science Division, Maywood, Illinois, United States of America.
authors.forename: Audrey
authors.initials: A
authors.lastname: Torcaso
authors.affiliation: Department of Cell and Molecular Physiology, Loyola University Chicago Health Science Division, Maywood, Illinois, United States of America.
authors.forename: Andrew
authors.initials: A
authors.lastname: Mariano
authors.affiliation: Department of Cell and Molecular Physiology, Loyola University Chicago Health Science Division, Maywood, Illinois, United States of America.
authors.forename: Li
authors.initials: L
authors.lastname: Xu
authors.affiliation: Department of Cell and Molecular Physiology, Loyola University Chicago Health Science Division, Maywood, Illinois, United States of America.
authors.forename: Sadia
authors.initials: S
authors.lastname: Mohsin
authors.affiliation: Department of Cell and Molecular Physiology, Loyola University Chicago Health Science Division, Maywood, Illinois, United States of America.
authors.forename: Lixia
authors.initials: L
authors.lastname: Zhao
authors.affiliation: Department of Cell and Molecular Physiology, Loyola University Chicago Health Science Division, Maywood, Illinois, United States of America.
authors.forename: Renzhi
authors.initials: R
authors.lastname: Han
mesh_terms: D000818:Animals; D000075368:Anoctamins; D002460:Cell Line; D049109:Cell Proliferation; D048049:Extracellular Signal-Regulated MAP Kinases / Q000378:metabolism; D055785:Gene Knockdown Techniques; D008810:Mice, Inbred C57BL; D018482:Muscle, Skeletal / Q000166:cytology; D032446:Myoblasts / Q000166:cytology* / Q000378:metabolism*; D049294:Phospholipid Transfer Proteins / Q000172:deficiency / Q000235:genetics / Q000378:metabolism*; D051057:Proto-Oncogene Proteins c-akt / Q000378:metabolism; D015398:Signal Transduction
chemical_list: C576687:ANO6 protein, mouse; D000075368:Anoctamins; D049294:Phospholipid Transfer Proteins; D051057:Proto-Oncogene Proteins c-akt; D048049:Extracellular Signal-Regulated MAP Kinases