Down‐regulated miR‐26a promotes proliferation, migration, and invasion via negative regulation of MTDH in esophageal squamous cell carcinoma

Abstract

Numerous studies have reported that the role played by miR-26a in cancer is controversial, but whether miR-26a regulates metadherin (MTDH) expression in esophageal squamous cell carcinoma (ESCC) is unclear. We performed this study to investigate the clinical relevance of miR-26a expression in ESCC. miR-26a was detected by using the hybridization method. To functionally analyze the role of miR-26a in ESCC cell lines, KYSE-450 and Eca109 cells were employed, whose endogenous miR-26a was artificially down- or up-regulated, respectively, by using lentiviral-based transfection. There was significant association between miR-26a expression and clinical stage ( = 0.049), lymph node metastasis ( = 0.023), tumor volume ( = 0.003), and poor overall prognosis ( = 0.026). miR-26a was able to suppress proliferation and migration of ESCC cells Moreover, we have confirmed that miR-26a can negatively regulate MTDH in ESCC cells by using luciferase reporter assay. In addition, to investigate the role miR-26a plays in cell proliferation, we nude mice were xenografted with ESCC cells whose miR-26a was stably down- and up-regulated. Together, our results show that miR-26a is capable of suppressing the proliferation and migration of ESCC cells negative regulation of MTDH. Moreover, miR-26a expression was clinically relevant in cancer progression and poor prognosis, which supports the idea that miR-26a acts as a tumor suppressor in ESCC.-Yang, C., Zheng, S., Liu, T., Liu, Q., Dai, F., Zhou, J., Chen, Y., Sheyhidin, I., Lu, X. Down-regulated miR-26a promotes proliferation, migration, and invasion negative regulation of MTDH in esophageal squamous cell carcinoma.

MicroRNA‐26a inhibits proliferation and tumorigenesis via targeting CKS2 in laryngeal squamous cell carcinoma

“…MiR‐26a has been implicated in multiple biological processes, such as proliferation, invasion, differentiation, angiogenesis and energy metabolism in cancer cells . It has been reported that inhibition of miR‐26a contributes to proliferation, migration and invasion via targeting metadherin in oesophageal squamous cell carcinoma .…”

“…26 It has been reported that inhibition of miR-26a contributes to proliferation, migration and invasion via targeting metadherin in oesophageal squamous cell carcinoma. 27 Overexpression of miR-26a reduced tumour cell growth of osteosarcoma in vitro and in vivo. 28 In ovarian cancer cells, reinforced expression of miR-26a inhibited proliferation and induced apoptosis.…”

miR‐26a inhibits proliferation and promotes apoptosis in porcine immature Sertoli cells by targeting the PAK2 gene

“…miR-26a-5p promoted chicken follicular theca cell proliferation and significantly up-regulated the expression of the anti-apoptotic BCL2 gene to inhibit apoptosis by targeting a trinucleotide repeat containing 6A gene (Kang et al, 2017). In addition, miR-26a also participates in regulating proliferation, apoptosis, migration, autophagy and invasion in multiple types of cancer cells, including vascular smooth muscle cells (Tan, Yang, Liu, & Yan, 2017), hepatocellular carcinoma cells (Jin et al, 2017;Li, Ren, et al, 2017), oesophageal squamous cell carcinoma cells Yang et al, 2017) and gastric cancer cells (Ding et al, 2017), (Correia et al, 2015;Kvansakul & Hinds, 2013;Mignard, Lalier, Paris, & Vallette, 2014;Volkmann, Marassi, Newmeyer, & Hanein, 2014). The anti-apoptotic proteins are located in the cytosol and are associated with the mitochondrial outer membrane, while the pro-apoptotic effector proteins are the mediators of mitochondrial outer membrane permeabilization (Correia et al, 2015;Mignard et al, 2014).…”

“…miR‐26a‐5p promoted chicken follicular theca cell proliferation and significantly up‐regulated the expression of the anti‐apoptotic BCL2 gene to inhibit apoptosis by targeting a trinucleotide repeat containing 6A gene (Kang et al, ). In addition, miR‐26a also participates in regulating proliferation, apoptosis, migration, autophagy and invasion in multiple types of cancer cells, including vascular smooth muscle cells (Tan, Yang, Liu, & Yan, ), hepatocellular carcinoma cells (Jin et al, ; Li, Ren, et al, ), oesophageal squamous cell carcinoma cells (Li, Liang, et al, ; Yang et al, ) and gastric cancer cells (Ding et al, ), by targeting different genes. In this study, miR‐26a overexpression arrested cells in G0/G1 phase, inhibited proliferation and promoted swine Sertoli cells apoptosis.…”

“…MicroRNAs (miRNAs), which are a class of non‐coding RNAs (approximately 22 nt in length), are widely detected in organisms and confirmed to regulate the expression of protein coding genes by targeting their 3′‐untranslated regions (3′‐UTRs; Figure a), thereby promoting mRNA degradation (perfect complementarity) or inhibiting mRNA translation (incomplete match). In the past years, miRNAs have been reported to participate in animal biological processes, including cell proliferation (Yao et al, ), cell apoptosis (Ma, Song, Yu, et al, ), autophagy (Jin et al, ), migration (Yang et al, ), organ development (Lian et al, ; Luo et al, ; Ran et al, ) and spermatogenesis (Procopio et al, ).…”