MicroRNA-107 inhibits proliferation and invasion of laryngeal squamous cell carcinoma cells by targeting CACNA2D1 in vitro

Huang, Chaoping; Wang, Zhenxiao; Zhang, Kun; Dong, Yanbo; Zhang, Aobo; Lu, Cheng Hsien; Liu, Liangfa

doi:10.1097/cad.0000000000000865

Cited by 24 publications

(18 citation statements)

References 32 publications

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“…Induced pluripotent stem cells (iPSCs) and HEK293T cells for spinocerebellar ataxia [ 302 ] Endostatin, zonisamide, clozapine, roscovitine, mibefradil, iron and zinc can block Cav3.1 channel [ 179 – 185 ] Dearomatized isoprenylated acylphloroglucinol and monoterpenoid, hypatone A could rescue pathological gating properties for spinocerebellar ataxia 42 [ 186 ] Autophagic pathway in melanoma cells [ 198 ] Apoptotic pathway in [ 193 – 195 ] Ras-ERK signaling pathway [ 200 , 201 ] CACNA1H Calcium voltage-gated channel subunit alpha1 H Cav3.2 T-type None TsA-201 cell for amyotrophic lateral sclerosis [ 303 ] KYS-05090S can block Cav3.2 current [ 187 ] Apoptotic pathway in myocardial cells [ 155 ]. Autophagy pathway [ 158 ] CACNA1I Calcium Voltage-Gated Channel Subunit Alpha1 I Cav 3.3 T-type HEK293T and mouse chromaffin cells for ID and epilepsy [ 74 ] None Zinc modulates Cav3.3 channel gating [ 181 ] None CACNA2D1 Calcium voltage-gated channel auxiliary subunit alpha2delta 1 Cav1.3 L-type None MKN74 cells (human gastric cancer cell line) [ 190 ] MicroRNA-107 can inhibit expression of Cav1.3 in cancer [ 188 , 189 ] Amlodipine can block Cav1.3 in cancer [ 190 ] CXCR3/ERK1/2 signaling pathway [ 203 ] Ras/Raf/MEK/ERK signaling pathway [ 202 ] …”

Section: Resultsmentioning

confidence: 99%

“…MicroRNA-107 can inhibit expression of Cav1.3 in cancer [ 188 , 189 ]…”

Section: Resultsmentioning

confidence: 99%

“…KYS-05090S could block Cav3.2 current [ 187 ]. Cav1.3 current could be blocked by microRNA-107 [ 188 , 189 ] and amlodipine [ 190 ]. The commonest affected pathway is apoptotic pathway [ 127 , 155 , 161 , 172 , 191 – 196 ] followed by autophagic pathway [ 158 , 197 – 199 ], Ras/Raf/MEK-ERK signaling pathway [ 200 – 203 ] and Wnt pathway [ 173 ].…”

Section: Summary Of the Clinical Featuresmentioning

confidence: 99%

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Calcium channelopathies and intellectual disability: a systematic review

Kessi

Chen

Peng

et al. 2021

Orphanet J Rare Dis

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Background Calcium ions are involved in several human cellular processes including corticogenesis, transcription, and synaptogenesis. Nevertheless, the relationship between calcium channelopathies (CCs) and intellectual disability (ID)/global developmental delay (GDD) has been poorly investigated. We hypothesised that CCs play a major role in the development of ID/GDD and that both gain- and loss-of-function variants of calcium channel genes can induce ID/GDD. As a result, we performed a systematic review to investigate the contribution of CCs, potential mechanisms underlying their involvement in ID/GDD, advancements in cell and animal models, treatments, brain anomalies in patients with CCs, and the existing gaps in the knowledge. We performed a systematic search in PubMed, Embase, ClinVar, OMIM, ClinGen, Gene Reviews, DECIPHER and LOVD databases to search for articles/records published before March 2021. The following search strategies were employed: ID and calcium channel, mental retardation and calcium channel, GDD and calcium channel, developmental delay and calcium channel. Main body A total of 59 reports describing 159 cases were found in PubMed, Embase, ClinVar, and LOVD databases. Variations in ten calcium channel genes including CACNA1A, CACNA1C, CACNA1I, CACNA1H, CACNA1D, CACNA2D1, CACNA2D2, CACNA1E, CACNA1F, and CACNA1G were found to be associated with ID/GDD. Most variants exhibited gain-of-function effect. Severe to profound ID/GDD was observed more for the cases with gain-of-function variants as compared to those with loss-of-function. CACNA1E, CACNA1G, CACNA1F, CACNA2D2 and CACNA1A associated with more severe phenotype. Furthermore, 157 copy number variations (CNVs) spanning calcium genes were identified in DECIPHER database. The leading genes included CACNA1C, CACNA1A, and CACNA1E. Overall, the underlying mechanisms included gain- and/ or loss-of-function, alteration in kinetics (activation, inactivation) and dominant-negative effects of truncated forms of alpha1 subunits. Forty of the identified cases featured cerebellar atrophy. We identified only a few cell and animal studies that focused on the mechanisms of ID/GDD in relation to CCs. There is a scarcity of studies on treatment options for ID/GDD both in vivo and in vitro. Conclusion Our results suggest that CCs play a major role in ID/GDD. While both gain- and loss-of-function variants are associated with ID/GDD, the mechanisms underlying their involvement need further scrutiny.

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Section: Resultsmentioning

confidence: 99%

“…MicroRNA-107 can inhibit expression of Cav1.3 in cancer [ 188 , 189 ]…”

Section: Resultsmentioning

confidence: 99%

Section: Summary Of the Clinical Featuresmentioning

confidence: 99%

See 1 more Smart Citation

Calcium channelopathies and intellectual disability: a systematic review

Kessi

Chen

Peng

et al. 2021

Orphanet J Rare Dis

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“…Abnormal proliferation is a unique feature of tumor cells andthe inhibition of tumor cell proliferation is controversial (23). miRNA serves an important role in tumorigenesis and the development of malignant tumors and regulates the proliferation and invasion of tumor cells by combining with target genes (24)(25)(26).…”

Section: Discussionmentioning

confidence: 99%

miR‑224‑5p regulates the proliferation, migration and invasion of pancreatic mucinous cystadenocarcinoma by targeting PTEN

Peng

Guo

et al. 2021

Mol Med Rep

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Pancreatic mucinous cystadenocarcinoma (MCC) is a rare malignant tumor, with a limited number of studies. The present study aimed to investigate the function and mechanism of microRNA (miR)-224-5p on proliferation, migration and invasion of MCC of the pancreas. Reverse transcription-quantitative PCR was used to explorethe expression of miR-224-5p and the PTEN gene. MTT, wound healing, Transwell and tumorigenesis assays were conducted to investigate the proliferation, migration and invasion of MCC1 cells in vitro and in vivo. Western blot analysis was employed to test the protein expression of PTEN. The target gene of miR-224-5p was assessed and verified by luciferase assay. miR-224-5p expression was notably higher, while PTEN expression was lower, in MCC1 cells compared with normal tissues and cells. Overexpression of miR-224-5p promoted the proliferation, migration and invasion of MCC and knockdown of miR-224-5p inhibited these functions. Bioinformatics analysis and luciferase assay indicated that PTEN was the direct target gene of miR-224-5p. The negative correlation between miR-224-5p and PTEN was confirmed both in vitro and in vivo. PTEN reversed the effects of miR-224-5p on proliferation, migration and invasion of MCC1 cells. The present study revealed for the first time, to the best of the authors' knowledge, that miR-224-5p was highly expressed and served an oncogenic role in MCC. miR-224-5p not only regulated the proliferation, migration and invasion of pancreatic MCC but may also be a potential therapeutic target for MCC.

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“…miR-107 suppressed let-7 expression and activated downstream oncoprotein expressions such as HMGA2 and RAS and enhanced the tumorigenic and metastatic potential of cancer cells [ 230 , 231 ]. In HNSCCs, a miR-107 increment was found in patients with lymph node metastasis, suggesting an oncogenic role for miR-107 [ 232 ]; however, miR-107 was indicated to suppress the proliferation, invasion, and colony formation of cells in LSCCs via inhibiting the voltage-gated calcium channel subunit α2δ1 (α2δ1) (encoded by CACNA2D1 ) [ 233 ]. In non-small-cell lung cancer (NSCLC), α2δ1 also enhances radioresistance in cancer stem-like cells by enhancing the efficiency of DNA damage repair [ 234 ].…”

Section: Mirnas In Regulating Cancer Stemnessmentioning

confidence: 99%

Roles of microRNAs in Regulating Cancer Stemness in Head and Neck Cancers

Fitriana

Hwang

Chan

et al. 2021

Cancers

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Head and neck squamous cell carcinomas (HNSCCs) are epithelial malignancies with 5-year overall survival rates of approximately 40–50%. Emerging evidence indicates that a small population of cells in HNSCC patients, named cancer stem cells (CSCs), play vital roles in the processes of tumor initiation, progression, metastasis, immune evasion, chemo-/radioresistance, and recurrence. The acquisition of stem-like properties of cancer cells further provides cellular plasticity for stress adaptation and contributes to therapeutic resistance, resulting in a worse clinical outcome. Thus, targeting cancer stemness is fundamental for cancer treatment. MicroRNAs (miRNAs) are known to regulate stem cell features in the development and tissue regeneration through a miRNA–target interactive network. In HNSCCs, miRNAs act as tumor suppressors and/or oncogenes to modulate cancer stemness and therapeutic efficacy by regulating the CSC-specific tumor microenvironment (TME) and signaling pathways, such as epithelial-to-mesenchymal transition (EMT), Wnt/β-catenin signaling, and epidermal growth factor receptor (EGFR) or insulin-like growth factor 1 receptor (IGF1R) signaling pathways. Owing to a deeper understanding of disease-relevant miRNAs and advances in in vivo delivery systems, the administration of miRNA-based therapeutics is feasible and safe in humans, with encouraging efficacy results in early-phase clinical trials. In this review, we summarize the present findings to better understand the mechanical actions of miRNAs in maintaining CSCs and acquiring the stem-like features of cancer cells during HNSCC pathogenesis.

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MicroRNA-107 inhibits proliferation and invasion of laryngeal squamous cell carcinoma cells by targeting CACNA2D1 in vitro

Cited by 24 publications

References 32 publications

Calcium channelopathies and intellectual disability: a systematic review

Calcium channelopathies and intellectual disability: a systematic review

miR‑224‑5p regulates the proliferation, migration and invasion of pancreatic mucinous cystadenocarcinoma by targeting PTEN

Roles of microRNAs in Regulating Cancer Stemness in Head and Neck Cancers

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