MiR‐133a‐3p Inhibits Oral Squamous Cell Carcinoma (OSCC) Proliferation and Invasion by Suppressing <i>COL1A1</i>

He, Baoxia; Lin, Xia; Feng-qi, Tian; Yu, Weijiang; Qiao, Bin

doi:10.1002/jcb.26182

Cited by 96 publications

(90 citation statements)

References 28 publications

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“…It has been discovered that miR‐133a‐3p acts as a tumor suppressor in bladder cancer (Gao et al, ). miR‐133a‐3p could also inhibit the migration and propagation of OSCC cells through decreasing COL1A1 expression (He et al, ). In this study, we discovered that miR‐133a‐3p was low‐expressed in ESCC.…”

Section: Discussionmentioning

confidence: 99%

miR‐133a‐3p suppresses cell proliferation, migration, and invasion and promotes apoptosis in esophageal squamous cell carcinoma

Yin

et al. 2018

Journal Cellular Physiology

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Objective This study aimed to investigate the expression levels of miR‐133a‐3p and collagen type I α 1 (COL1A1) in esophageal squamous cell carcinoma (ESCC) to find out the relationship between miR‐133a‐3p and COL1A1 and their influence on ESCC propagation, migration, invasion, and apoptosis. Methods The messenger RNA expression levels of miR‐133a‐3p and COL1A1 in ESCC were detected by quantitative reverse‐transcription polymerase chain reaction. The expression of COL1A1 protein was examined via western blot analysis and immunohistochemistry assay. Cell propagation and apoptosis were, respectively, confirmed by CCK‐8 and flow cytometry assay, whereas cell mobility and invasiveness were analyzed by wound healing assay and transwell assay. The targeted relationship between miR‐133a‐3p and COL1A1 was validated by the dual luciferase reporter assay. The tumor xenograft model was constructed to further verify the impact of miR‐133a‐3p on esophageal squamous tumor growth and COL1A1 expression in vivo. Results miR‐133a‐3p was found low‐expressed whereas COL1A1 was highly expressed in esophageal squamous cancer tissue and cells. The expression of miR‐133a‐3p was negatively correlated with COL1A1 expression. The dual luciferase reporter gene assay confirmed that miR‐133a‐3p directly targeted COL1A1 and suppressed its expression. Cell Counting Kit‐8 assay, transwell assay, and flow cytometry analysis demonstrated that COL1A1 promoted ESCC propagation and invasion and suppressed cell apoptosis, whereas miR‐133a‐3p reversed such adverse effects by regulating COL1A1. Conclusions miR‐133a‐3p inhibited the cell propagation, invasion, and migration and facilitated apoptosis in ESCC by targeting COL1A1.

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Section: Discussionmentioning

confidence: 99%

miR‐133a‐3p suppresses cell proliferation, migration, and invasion and promotes apoptosis in esophageal squamous cell carcinoma

Yin

et al. 2018

Journal Cellular Physiology

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“…Our data illustrated that miR-133a-3p downregulated and promoted its targets such as EGFR and HuR in HPV(+) tissues and cells. Of note, miR-133a-3p has been reported to inhibit proliferation and migration of HNSCC cells through targeting COL1A1 and repressing its expression [ 30 ].…”

Section: Discussionmentioning

confidence: 99%

Smoking-induced control of miR-133a-3p alters the expression of EGFR and HuR in HPV-infected oropharyngeal cancer

et al. 2018

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PurposeHuman papillomavirus (HPV) infected oropharyngeal squamous cell carcinoma (OPSCC) patients have a better prognosis compared to HPV(-) counterparts. However, a subset of HPV(+) patients with a smoking history fail to respond to the standard of care treatments such as radiation and chemotherapy. To understand the underlying mechanism driving HPV(+) OPSCC patient resistance to treatment and recurrence, we sought to identify and characterize the differentially expressed miRNAs and their target genes in HPV(+) smokers and non-smokers.Experimental designMicroRNA expression analysis was performed using Nanostring in tumor tissues isolated from a prospective cohort of HPV(+) smoking (n = 9) and HPV(+) (n = 13) non-smoking OPSCC patients. Identified miRNAs of interest were further validated using qRT-PCR in cigarette smoke extract (CSE) treated HPV(+) and E6/E7 overexpressing HPV(-) cells.ResultsIn comparison to OPSCC HPV(+) non-smokers, 38 miRNAs were significantly altered in the HPV(+) smoker patients cohort and out of that 9 were downregulated. Altered miRNA expression was also detected in the serum and metastatic lymph nodes of HPV(+) smokers versus non-smokers. Expression of miR-133a-3p was significantly downregulated in OPSCC smokers, HPV(+) cells and E6/E7 overexpressing HPV(-) cells treated with CSE. Reduction of miR-133a-3p induced the upregulation of miR-133a-3p target mRNAs EGFR and HuR.ConclusionsOur results indicate that miR-133a-3p is a target of smoking-induced changes in HPV(+) patients and alters the expression of EGFR and HuR which may promote HPV associated oropharyngeal cancer. Therefore, future treatment strategies for HPV(+) OPSCC smokers should focus on EGFR inhibition and the development of selective therapies to target HuR.

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“…Hunsaker et al (2019) [75] studied the effect of the addition of melatonin to culture on exosomal expression of the OSCC-associated microRNAs, miR-21 miR-133a and miR-155, in the OSCC cell lines SSC25, CAL27 and SSC9. Increased expression of both miR-21 [76] and miR-155 [76] have been associated with poor prognosis, whereas miR-133-3p has been reported to inhibit OSCC in vitro [77]. Exosomal miRNA expression assessed by qPCR following addition of melatonin found significantly increased expression of miR-21 from all three cell lines (p < 0.05), significant reduction of miR-155 expression (p < 0.05), but no impact on miR-133a expression [75].…”

Section: Therapeutic Influence On Oscc-evsmentioning

confidence: 99%

Extracellular Vesicles in Oral Squamous Cell Carcinoma and Oral Potentially Malignant Disorders: A Systematic Review

Yap

Pruthi

Seers

et al. 2020

IJMS

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Extracellular vesicles (EVs) are secreted from most cell types and utilized in a complex network of near and distant cell-to-cell communication. Insight into this complex nanoscopic interaction in the development, progression and treatment of oral squamous cell carcinoma (OSCC) and precancerous oral mucosal disorders, termed oral potentially malignant disorders (OPMDs), remains of interest. In this review, we comprehensively present the current state of knowledge of EVs in OSCC and OPMDs. A systematic literature search strategy was developed and updated to December 17, 2019. Fifty-five articles were identified addressing EVs in OSCC and OPMDs with all but two articles published from 2015, highlighting the novelty of this research area. Themes included the impact of OSCC-derived EVs on phenotypic changes, lymph-angiogenesis, stromal immune response, mechanisms of therapeutic resistance as well as utility of EVs for drug delivery in OSCC and OPMD. Interest and progress of knowledge of EVs in OSCC and OPMD has been expanding on several fronts. The oral cavity presents a unique and accessible microenvironment for nanoparticle study that could present important models for other solid tumours.

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MiR‐133a‐3p Inhibits Oral Squamous Cell Carcinoma (OSCC) Proliferation and Invasion by Suppressing COL1A1

Cited by 96 publications

References 28 publications

miR‐133a‐3p suppresses cell proliferation, migration, and invasion and promotes apoptosis in esophageal squamous cell carcinoma

miR‐133a‐3p suppresses cell proliferation, migration, and invasion and promotes apoptosis in esophageal squamous cell carcinoma

Smoking-induced control of miR-133a-3p alters the expression of EGFR and HuR in HPV-infected oropharyngeal cancer

Extracellular Vesicles in Oral Squamous Cell Carcinoma and Oral Potentially Malignant Disorders: A Systematic Review

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