Abstract
Anoctamin-1 (ANO1), also known as TMEM16A, is the most studied member of anoctamin family of calcium-activated chloride channels with diverse cellular functions. ANO1 controls multiple cell functions including cell proliferation, survival, migration, contraction, secretion, and neuronal excitation. This review summarizes the current knowledge of the cellular mechanisms governing the regulation of ANO1 expression and of ANO1-mediated intracellular signaling. This includes the stimuli and mechanisms controlling ANO1 expression, agonists and processes that activate ANO1, and signal transduction mediated by ANO1. The major conclusion is that this field is poorly understood, remains highly controversial, and requires extensive and rigorous further investigation.
Highlights
Anoctamin-1 (ANO1), known as TMEM16A, DOG1 (Discovered On Gastrointestinal stromal tumors 1), ORAOV2 (Oral cancer Overexpressed), and TAOS-2 (Tumor Amplified and Overexpressed) was initially found to be overexpressed in a number of cancer tissues and is thought to contribute to cancer cell growth and tumorigenesis (Bill and Alex Gaither, 2017; Crottes and Jan, 2019)
The most recognized cellular functions of ANO1 include the control of cancer cell proliferation, survival and migration by ANO1 (Bill and Alex Gaither, 2017; Crottes and Jan, 2019), secretory function of ANO1 in the epithelia, such as airways, intestines, salivary glands, renal tubules and sweat glands (Jang and Oh, 2014), induction of electrical pacemaker activity of interstitial cells of Cajal in gastrointestinal smooth muscles (Sanders et al, 2012), control of acute pain sensation, chronic pain and anxiety-related behaviors (Oh and Jung, 2016; Cho et al, 2020), and contribution
This review summarizes the current knowledge of mechanisms governing the regulation of ANO1 expression and ANO1-induced intracellular signaling
Summary
Anoctamin-1 (ANO1), known as TMEM16A, DOG1 (Discovered On Gastrointestinal stromal tumors 1), ORAOV2 (Oral cancer Overexpressed), and TAOS-2 (Tumor Amplified and Overexpressed) was initially found to be overexpressed in a number of cancer tissues and is thought to contribute to cancer cell growth and tumorigenesis (Bill and Alex Gaither, 2017; Crottes and Jan, 2019). Epidermal growth factor (EGF) promotes ANO1 expression in colonic epithelial cancer cells (Mroz and Keely, 2012) and in breast cancer cells (Wang et al, 2019). ANO1 expression was transiently induced by the bacterial toxin lipopolysaccharide (LPS) in human lung adenocarcinoma A549 cells (Zhang et al, 2014), in cultured mouse lung cancer cell line LA795, and in mouse alveolar epithelial cells in vivo after intraperitoneal injection of LPS (Li H. et al, 2016). STAT3 is important for ANO1 transcription in response to IL-6 in pancreatic acinar cells (Wang et al, 2020) and in response to EGF in breast cancer cells (Wang et al, 2019). EGF-induced ANO1 expression in colonic epithelial cancer cells was dependent on the activity of protein kinase C-δ (PKCδ) and phosphatidylinositol 3-kinase (PI3K), but the link to STAT3 was not investigated (Mroz and Keely, 2012). ANO1 expression was reported to be dependent on STAT6 in human bronchial epithelial cells
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
