Suppression of T-Type Ca2+ Channels Inhibited Human Laryngeal Squamous Cell Carcinoma Cell Proliferation Running Title: Roles of T-Type Ca2+ Channels in LSCC Cell Proliferation

Yu, Wenfa; Wang, Ping; Ma, Huiming; Zhang, Guozheng; Zhao, Yue; Lu, Baocai; Wang, Huiming; Dong, Mingmin

doi:10.7754/clin.lab.2013.130614

Cited by 14 publications

(11 citation statements)

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“…Similarly, Ca V 3.1 channel expression was present in human laryngeal squamous cell carcinoma tissue and cell lines [ 94 ]. Notably, CACNA1G gene knock-down and the Ca V 3 channel blocker, mibefradil, significantly reduced the rate of cell proliferation in this cancer [ 94 ].…”

Section: Voltage-gated Calcium Channelsmentioning

confidence: 99%

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Voltage-Gated Ion Channels in Cancer Cell Proliferation

Rao¹,

Perez-Neut²,

Kaja³

et al. 2015

Cancers

168

160

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Changes of the electrical charges across the surface cell membrane are absolutely necessary to maintain cellular homeostasis in physiological as well as in pathological conditions. The opening of ion channels alter the charge distribution across the surface membrane as they allow the diffusion of ions such as K+, Ca++, Cl−, Na+. Traditionally, voltage-gated ion channels (VGIC) are known to play fundamental roles in controlling rapid bioelectrical signaling including action potential and/or contraction. However, several investigations have revealed that these classes of proteins can also contribute significantly to cell mitotic biochemical signaling, cell cycle progression, as well as cell volume regulation. All these functions are critically important for cancer cell proliferation. Interestingly, a variety of distinct VGICs are expressed in different cancer cell types, including metastasis but not in the tissues from which these tumors were generated. Given the increasing evidence suggesting that VGIC play a major role in cancer cell biology, in this review we discuss the role of distinct VGIC in cancer cell proliferation and possible therapeutic potential of VIGC pharmacological manipulation.

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Section: Voltage-gated Calcium Channelsmentioning

confidence: 99%

“…One recent study demonstrated that while nifedipine promoted both the proliferation and migration of breast cancer in vitro and in vivo [ 91 ], verapamil did not affect proliferation [ 91 ]. The Cav3 inhibitors including mibefradil are able to inhibit cancer cell proliferation [ 94 , 96 ].…”

Section: Vgics As Therapeutic Targets For Cancermentioning

confidence: 99%

Voltage-Gated Ion Channels in Cancer Cell Proliferation

Rao¹,

Perez-Neut²,

Kaja³

et al. 2015

Cancers

168

160

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“…Soon however, it was demonstrated that mibefradil also inhibits K + channels (e.g., Liu et al, ; Perchenet and Clement‐Chomienne, ; Hong et al, ). On the other hand, recent reports credit mibefradil as a drug endowed with tumor suppressing activity, arising from its inhibitory effect on Ca 2+ channels (e.g., Keir et al, ; Sheehan et al, ; Valerie et al, ; Yu et al, ; Rao et al, ). Therefore, and considering its reported effects on K + channels, we decided to study the interaction between mibefradil and the tumor‐related Kv10.1 channel (e.g., Meyer and Heinemann, ; Liu et al, ; Pardo et al, ; Hemmerlein et al, ; Stühmer et al, ; Pardo and Stühmer, , ; Agarwal et al, ).…”

mentioning

confidence: 99%

Gating Modulation of the Tumor‐Related Kv10.1 Channel by Mibefradil

Gómez-Lagunas

Carrillo

Pardo

et al. 2017

Journal Cellular Physiology

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Several reports credit mibefradil with tumor suppressing properties arising from its known inhibition of Ca currents. Given that mibefradil (Mb) is also known to inhibit K channels, we decided to study the interaction between this organic compound and the tumor-related Kv10.1 channel. Here we report that Mb modulates the gating of Kv10.1. Mb induces an apparent inactivation from both open and early closed states where the channels dwell at hyperpolarized potentials. Additionally, Mb accelerates the kinetics of current activation, in a manner that depends on initial conditions. Our observations suggest that Mb binds to the voltage sensor domain of Kv10.1 channels, thereby modifying the gating of the channels in a way that in some, but not all, aspects opposes to the gating effects exerted by divalent cations. J. Cell. Physiol. 232: 2019-2032, 2017. © 2016 Wiley Periodicals, Inc.

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“…Targeting calcium signaling can reactivate tumor suppressor genes silenced by calciumcalmodulin kinase and increase cell death in colon cancer (Raynal et al 2016). Moreover, suppression of Ca2+ channels has be showed to inhibit the proliferation of LSCC cell line in vitro (Yu et al 2014). However，to date there are very few studies on calcium signaling in LSCC.…”

Section: Discussionmentioning

confidence: 99%

Peer Review #2 of "Construction and integrated analysis of crosstalking ceRNAs networks in laryngeal squamous cell carcinoma (v0.1)"

Lu¹

2019

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Background: Laryngeal squamous cell carcinoma (LSCC) is one of the most common malignant tumours of the head and neck. Recent evidence has demonstrated that lncRNAs play important roles in tumour progression and could be used as biomarkers for early diagnosis, prognosis, and potential therapeutic targets. The "competitive endogenous RNA (ceRNA)" hypothesis states that lncRNAs competitively bind to miRNAs through their intramolecular miRNA reaction elements (MREs) to construct a wide range of ceRNA regulatory networks. This study aims to predict the role of ceRNA network in LSCC, for advancing the understanding of underlying mechanisms of tumorigenesis. Material and Methods: In this study, the functions of lncRNAs as ceRNAs in LSCC and their prognostic significance were investigated via comprehensive integrated expression profiles data of lncRNAs, mRNAs, and miRNAs obtained from The Cancer Genome Atlas (TCGA). Protein-protein interaction, gene ontology, pathway, and Kaplan-Meier curves analysis were used to profile the expression and function of altered RNAs in LSCC Results: As a result, 889 lncRNAs, 55 miRNAs and 1946 mRNAs were found to be differentially expressed in LSCC. These altered mRNAs were mainly involved in extracellular matrix organization, calcium signaling, and metabolic pathways. To study the regulatory function of lncRNAs, an lncRNAmediated ceRNA network was constructed. This ceRNA network included 61 lncRNAs, 7 miRNAs and 7 target mRNAs. Of these RNAs, lncRNAs (TSPEAR-AS, CASK-AS1, MIR137HG, PART1, LSAMP-AS1), miRNA (has-mir-210) and mRNAs (HOXC13, STC2, DIO1, FOXD4L1) had a significant effect on the prognosis of LSCC. Conclusion: The results of this study broaden the understanding of the mechanisms by which lncRNAs are involved in tumorigenesis. Furthermore, five lncRNAs (TSPEAR-AS，CASK-AS1, MIR137HG, PART1, LSAMP-AS1) were identified as potential prognostic biomarkers and therapeutic targets for LSCC. These results provide a basis for further experimental and clinical research.

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Suppression of T-Type Ca2+ Channels Inhibited Human Laryngeal Squamous Cell Carcinoma Cell Proliferation Running Title: Roles of T-Type Ca2+ Channels in LSCC Cell Proliferation

Cited by 14 publications

References 0 publications

Voltage-Gated Ion Channels in Cancer Cell Proliferation

Voltage-Gated Ion Channels in Cancer Cell Proliferation

Gating Modulation of the Tumor‐Related Kv10.1 Channel by Mibefradil

Peer Review #2 of "Construction and integrated analysis of crosstalking ceRNAs networks in laryngeal squamous cell carcinoma (v0.1)"

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