miR-200c-3p spreads invasive capacity in human oral squamous cell carcinoma microenvironment

Tomoyo Kawakubo-Yasukochi, Masahiko Morioka, Mai Hazekawa, Atsushi Yasukochi, Takuya Nishinakagawa, Kazuhiko Ono, Shintarou Kawano, Seiji Nakamura, Manabu Nakashima

Research output: Contribution to journalArticle

7 Citations (Scopus)

Abstract

Oral squamous cell carcinoma (OSCC) constitutes over 90% of all cancers in the oral cavity. The prognosis for patients with invasive OSCC is poor; therefore, it is important to understand the molecular mechanisms of invasion and subsequent metastasis not only to prevent cancer progression but also to detect new therapeutic targets against OSCC. Recently, extracellular vesicles—particularly exosomes—have been recognized as intercellular communicators in the tumor microenvironment. As exosomic cargo, deregulated microRNAs (miRNAs) can shape the surrounding microenvironment in a cancer-dependent manner. Previous studies have shown inconsistent results regarding miR-200c-3p expression levels in OSCC cell lines, tissues, or serum—likely because of the heterogeneous characters of the specimen materials. For this reason, single-cell clone analyses are necessary to effectively assess the role of exosome-derived miRNAs on cells within the tumor microenvironment. The present study utilized integrated microarray profiling to compare exosome-derived miRNA and exosome-treated cell-derived mRNA expression. Data were acquired from noninvasive SQUU-A and highly invasive SQUU-B tongue cancer cell clones derived from a single patient to determine candidate miRNAs that promote OSCC invasion. Matrigel invasion assays confirmed that hsa-miR-200c-3p was a key pro-invasion factor among six miRNA candidates. Consistently, silencing of the miR-200c-3p targets, CHD9 and WRN, significantly accelerated the invasive potential of SQUU-A cells. Thus, our data indicate that miR-200c-3p in exosomes derived from a highly invasive OSCC line can induce a similar phenotype in non-invasive counterparts.

Original languageEnglish
Pages (from-to)295-302
Number of pages8
JournalMolecular Carcinogenesis
Volume57
Issue number2
DOIs
Publication statusPublished - Feb 1 2018

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Cellular Microenvironment
Exosomes
Squamous Cell Carcinoma
MicroRNAs
Tumor Microenvironment
Tongue Neoplasms
Single-Cell Analysis
Cell Line
Mouth Neoplasms
Mouth
Neoplasms
Clone Cells
Neoplasm Metastasis
Phenotype
Messenger RNA

All Science Journal Classification (ASJC) codes

  • Molecular Biology
  • Cancer Research

Cite this

Kawakubo-Yasukochi, T., Morioka, M., Hazekawa, M., Yasukochi, A., Nishinakagawa, T., Ono, K., ... Nakashima, M. (2018). miR-200c-3p spreads invasive capacity in human oral squamous cell carcinoma microenvironment. Molecular Carcinogenesis, 57(2), 295-302. https://doi.org/10.1002/mc.22744

miR-200c-3p spreads invasive capacity in human oral squamous cell carcinoma microenvironment. / Kawakubo-Yasukochi, Tomoyo; Morioka, Masahiko; Hazekawa, Mai; Yasukochi, Atsushi; Nishinakagawa, Takuya; Ono, Kazuhiko; Kawano, Shintarou; Nakamura, Seiji; Nakashima, Manabu.

In: Molecular Carcinogenesis, Vol. 57, No. 2, 01.02.2018, p. 295-302.

Research output: Contribution to journalArticle

Kawakubo-Yasukochi, T, Morioka, M, Hazekawa, M, Yasukochi, A, Nishinakagawa, T, Ono, K, Kawano, S, Nakamura, S & Nakashima, M 2018, 'miR-200c-3p spreads invasive capacity in human oral squamous cell carcinoma microenvironment', Molecular Carcinogenesis, vol. 57, no. 2, pp. 295-302. https://doi.org/10.1002/mc.22744
Kawakubo-Yasukochi T, Morioka M, Hazekawa M, Yasukochi A, Nishinakagawa T, Ono K et al. miR-200c-3p spreads invasive capacity in human oral squamous cell carcinoma microenvironment. Molecular Carcinogenesis. 2018 Feb 1;57(2):295-302. https://doi.org/10.1002/mc.22744
Kawakubo-Yasukochi, Tomoyo ; Morioka, Masahiko ; Hazekawa, Mai ; Yasukochi, Atsushi ; Nishinakagawa, Takuya ; Ono, Kazuhiko ; Kawano, Shintarou ; Nakamura, Seiji ; Nakashima, Manabu. / miR-200c-3p spreads invasive capacity in human oral squamous cell carcinoma microenvironment. In: Molecular Carcinogenesis. 2018 ; Vol. 57, No. 2. pp. 295-302.
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