The effects of transient receptor potential channel (TRPC) on airway smooth muscle cell isolated from asthma model mice

Zhang, Xiaoyu; Zhao, Zhixin; Ma, Lijun; Guo, Yu; Li, Xiaosu; Zhao, Limin; Tian, Cui-jie; Tang, Xue-yi; Cheng, Dongjun; Chen, Zhuochang; Zhang, Luoxian

doi:10.1002/jcb.26801

Cited by 11 publications

(13 citation statements)

References 30 publications

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“…TRPC1, one of the TRPC channels, is expressed in almost all tissues and various tumors. Many studies have demonstrated that the TRPC1 channel plays an important role in tumor cell proliferation, differentiation, apoptosis, migration, and invasion in distinct kinds of tumors, including breast cancer, prostate cancer, gastric cancer, and liver cancer (7)(8)(9)(10)(11)(12)(20)(21)(22). The abnormal expression of TRPC1 can accelerate the uncontrolled proliferation and invasion of tumor cells.…”

Section: Discussionmentioning

confidence: 99%

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TRPC1 Inhibits Cell Proliferation/Invasion and Is Predictive of a Better Prognosis of Esophageal Squamous Cell Carcinoma

et al. 2021

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Background and ObjectivesIn China, over 90% of esophageal cancer (EC) cases are esophageal squamous cell carcinoma (ESCC). ESCC is a frequently malignant tumor with poor prognosis despite the development of comprehensive therapeutic strategies, for which there is still a lack of effective prognostic factors. Previous studies found that the abnormal expression of TRPC1 is closely related to the proliferation, invasion, metastasis, and differentiation of various tumors. However, the relationship between TRPC1 and ESCC is currently unclear. The present study aimed to clarify the clinical significance of TRPC1 and to preliminarily assess the molecular mechanism by which TRPC1 regulates cell proliferation, migration, and invasion in ESCC.Materials and MethodsImmunohistochemistry (IHC) was used to determine the expression of TRPC1 and Ki-67 in 165 cases of ESCC. The correlations between TRPC1 expression and clinicopathological characteristics were determined, and both univariate and multivariate analyses were utilized to quantify the impact of TRPC1 expression on patient survival. Cell Counting Kit-8, scratch wound healing, and transwell assays were used to determine the effects of TRPC1 on proliferation, migration, and invasion in ESCC in vitro, respectively.ResultsThe positive expression rate of TRPC1 showed significantly decreased in ESCC (45.50%) compared with the levels in normal esophageal mucosa (NEM; 80.80%) and high-grade intraepithelial neoplasia (HGIEN; 63.20%) (P<0.001). Higher expression rate of TRPC1 was associated with low lymph node metastasis (P<0.001), high differentiation (rs= 0.232, P=0.003), and low Ki-67 (rs = −0.492, P<0.001). We further revealed that low expression of TRPC1 was associated with poor prognosis (Disease-free survival, DFS: 95% CI=0.545–0.845, P=0.001; Overall survival, OS: 95% CI=0.553–0.891, P=0.004). Furthermore, we showed that downregulation of TRPC1 promoted the proliferation, migration, and invasion of human esophageal squamous cell carcinoma cell line EC9706 in vitro. In contrast, overexpression of TRPC1 inhibited the proliferation, migration, and invasion of human esophageal squamous cell carcinoma cell line KYSE150 (P<0.01), in a manner at least in part mediated through the AKT/p27 pathway.ConclusionTRPC1 inhibited the proliferation, migration, and invasion of EC9706 and KYSE150 cells, at least, in part mediated through the AKT/p27 pathway in vitro. The downregulation of TRPC1 may be one of the most important molecular events in the malignant progression of ESCC. TRPC1 could be a new candidate tumor suppressor gene and a new prognostic factor of ESCC.

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Section: Discussionmentioning

confidence: 99%

“…The expression of TRPC1 had been extensively studied in various types of tissue or tumor. The abnormal expression of TRPC1 was found to be involved in tumor growth, migration, invasion, and differentiation (7)(8)(9)(10)(11)(12).…”

Section: Introductionmentioning

confidence: 99%

TRPC1 Inhibits Cell Proliferation/Invasion and Is Predictive of a Better Prognosis of Esophageal Squamous Cell Carcinoma

et al. 2021

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“…The TRP channels superfamily can be divided into seven subfamilies based on sequence homology: TRPA (ANKTM1), TRPC (canonical), TRPM (melastatin), TRPML (mucolipidins), TRPN (NompC), TRPV (vanil) and TRPP (polycystin) [ 48 ]. Transient receptor potential canonical (TRPC) channels belong to the TRP superfamily and most of them expressed in ASM [ 49 , 50 ]. They may mediated changes in [Ca 2+ ] i and induced ASM abnormal contraction, proliferation, hypertrophy, as well as secretion of inflammatory mediators [ 41 , 51 ].…”

Section: Regulation Of Trp Channels In the Function Of Asmmentioning

confidence: 99%

Roles of airway smooth muscle dysfunction in chronic obstructive pulmonary disease

et al. 2018

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The airway smooth muscle (ASM) plays an indispensable role in airway structure and function. Dysfunction in ASM plays a central role in the pathogenesis of chronic obstructive pulmonary disease (COPD) and contributes to alterations of contractility, inflammatory response, immunoreaction, phenotype, quantity, and size of airways. ASM makes a key contribution in COPD by various mechanisms including altered contractility and relaxation induce by [Ca2+]i, cell proliferation and hypertrophy, production and modulation of extracellular cytokines, and release of pro-and-anti-inflammatory mediators. Multiple dysfunctions of ASM contribute to modulating airway responses to stimuli, remodeling, and fibrosis, as well as influence the compliance of lungs. The present review highlights regulatory roles of multiple factors in the development of ASM dysfunction in COPD, aims to understand the regulatory mechanism by which ASM dysfunctions are initiated, and explores the clinical significance of ASM on alterations of airway structure and function in COPD and development of novel therapeutic strategies for COPD.

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“…TRPC-1 and TRPC-3 regulate the movement of cations, particularly Ca ++ , across cell membranes to activate Ca ++ -dependent processes. [50][51][52][53] They participate in the formation of store operated calcium channels (SOCC) that maintain cytoplasmic and sarcoplasmic/endoplasmic reticulum Ca ++ balance. Ca ++ channels control the progression of ASM cells through the cell cycle, reducing the levels of phosphorylated p38 mitogen activated protein kinase (p38 MAPK), Jun n-Terminal Kinase (JNK) and Bcl-2, and increase cell survival through decreased caspase 3 cleavage.…”

mentioning

confidence: 99%

“…Ca ++ channels control the progression of ASM cells through the cell cycle, reducing the levels of phosphorylated p38 mitogen activated protein kinase (p38 MAPK), Jun n-Terminal Kinase (JNK) and Bcl-2, and increase cell survival through decreased caspase 3 cleavage. 50 TNF-α and IL-1β modulate inflammatory processes in chronic asthma and during acute exacerbations. IL-1β treatment of human ASM cells enhances the activities of other mediators such as IL-4, IL-5, IL-13, and leukotrienes.…”

mentioning

confidence: 99%

Targeting Airway Smooth Muscle Hypertrophy in Asthma: An Approach Whose Time Has Come

Chetty¹,

Nielsen²

2021

JAA

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Airway smooth muscle (ASM) cell dysfunction is an important component of several obstructive pulmonary diseases, particularly asthma. External stimuli such as allergens, dust, air pollutants, and change in environmental temperatures provoke ASM cell hypertrophy, proliferation, and migration without adequate mechanistic controls. ASM cells can switch between quiescent, migratory, and proliferative phenotypes in response to extracellular matrix proteins, growth factors, and other soluble mediators. While some aspects of airway hypertrophy and remodeling could have beneficial effects, in many cases these contribute to a clinical phenotype of difficult to control asthma. In this review, we discuss the factors responsible for ASM hypertrophy and proliferation in asthma, focusing on cytokines, growth factors, and ion transporters, and discuss existing and potential approaches that specifically target ASM hypertrophy to reduce the ASM mass and improve asthma symptoms. The goal of this review is to highlight strategies that appear ready for translational investigations to improve asthma therapy.

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The effects of transient receptor potential channel (TRPC) on airway smooth muscle cell isolated from asthma model mice

Cited by 11 publications

References 30 publications

TRPC1 Inhibits Cell Proliferation/Invasion and Is Predictive of a Better Prognosis of Esophageal Squamous Cell Carcinoma

TRPC1 Inhibits Cell Proliferation/Invasion and Is Predictive of a Better Prognosis of Esophageal Squamous Cell Carcinoma

Roles of airway smooth muscle dysfunction in chronic obstructive pulmonary disease

Targeting Airway Smooth Muscle Hypertrophy in Asthma: An Approach Whose Time Has Come

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