Background: This study was aimed to evaluate the involvement of lncRNA MALAT1 in modifying chemo-sensitivity of laryngeal squamous cell carcinoma (LSCC) cell lines.
Methods: Totally 108 pairs of tumor tissues and matched para-tumor normal tissues were gathered from patients who were pathologically confirmed as LSCC. Meanwhile, LSCC cell lines, including TU686, TU177, AMC-HN-8, and LSC-1, were purchased to evaluate their tolerance to cisplatin, 5-fluorouracil, paclitaxel, and vincristine. Additionally, CCK-8 assay, flow cytometry, transwell assay, and wound healing assay were implemented to assess the part of MALAT1 in modulating viability, apoptosis, invasion, and migration of LSCC cell lines.
Results: MALAT1 expression was higher in LSCC tissues than in adjacent normal tissues (P < .05), and LSCC patients who carried highly expressed MALAT1 demonstrated poorer 5-year survival than ones with low MALAT1 expression (P < .05). For another, expression of MALAT1 was also unusually elevated within TU686, TU177, AMC-HN-8, and LSC-1 cell lines as relative to NHBEC cell line (P < .05). The TU686 cell line therein excelled in resisting the growth-curbing effects of 5-fluorouracil (IC50 = 20.44 μmol/L), paclitaxel (IC50 = 35.86 μg/L), and vincristine (IC50 = 0.12 μmol/L), when compared with TU177, AMC-HN-8, and LSC-1 cell line (P < .05). Moreover, there seemed great potential for over-expressed MALAT1 to enhance the chemo-resistance of both TU686 and LSC-1 cell lines (P < .05). Not only that, silencing of MALAT1 tended to undermine the proliferative and metastatic power of TU686 and LSC-1 cell lines (P < .05).
Conclusion: LncRNA MALAT1 counted in triggering tolerance of LSCC against chemo-drugs by boosting metastasis and depressing apoptosis of tumor cells.
Keywords: LncRNA MALAT1; chemo-sensitivity; epithelial-mesenchymal transition; laryngeal squamous cell carcinoma.
© 2019 The Authors. Journal of Clinical Laboratory Analysis published by Wiley Periodicals, Inc.