Long non-coding RNA small nucleolar RNA host gene 7 facilitates the proliferation, migration, and invasion of esophageal cancer cells by regulating microRNA-625

Abstract

Background: Esophageal cancer (EC) is a highly aggressive malignant tumor, of which esophageal squamous cell carcinoma (ESCC) constitutes the main subtype. Long non-coding RNA (lncRNA) small nucleolar RNA host gene 7 (SNHG7) has been extensively studied in many tumors and has been confirmed to be an oncogene; however, it has yet to be investigated in an ESCC study. Therefore, this study intended to uncover the role of SNHG7 in ESCC.Methods: Quantitative real-time polymerase chain reaction was applied to measure the expression levels of SNHG7 and miR-625 in ESCC tumor tissues and cell lines. Cell Counting Kit-8 assay, 5-Ethynyl-2'deoxyuridine assay, scratch assay, and Transwell assay were conducted to assess the proliferation, migration, and invasion ESCC cell. We verified the interaction between SNHG7 and miR-625 by performing the dual luciferase reporter gene experiment.Results: Compared to that in adjacent normal tissues and HET1A cell lines, the expression level of SNHG7 in ESCC tumor tissues and ESCC cell lines was up-regulated, while the expression level of miR-625 was down-regulated. ESCC cell proliferation, migration, and invasion were significantly promoted by SNHG7 overexpression but inhibited by silencing of SNHG7. Further, luciferase reporter gene experiments confirmed that SNHG7 interacted with miR-625, and rescue experiments showed that SNHG7 promoted the malignant phenotype by inhibiting miR-625.Conclusions: SNHG7 is up-regulated in ESCC tumor tissues and cell lines, while miR-625 is expressed at a low level. SNHG7 is able to facilitate the proliferation, migration, and invasion of ESCC cells by targeting miR-625.

The knockdown of lncRNA DLGAP1‐AS2 suppresses osteosarcoma progression by inhibiting aerobic glycolysis via the miR‐451a/HK2 axis

“…Wild‐type DLGAP1‐AS2 and the mutant‐type DLGAP1‐AS2 were cloned into the firefly luciferase gene reporter vector pmirGLO (Promega). The pmirGLO‐DLGAP1‐AS2‐WT or pmirGLO‐DLGAP1‐AS2‐MUT was co‐transfected into U2OS and Soas2 cells with miR‐451a mimics or NC mimics for 48 h, and then detected using the luciferase reporter assay system (Promega) 25 . Similarly, wild‐type HK2 and mutant‐type HK2 were cloned into the firefly luciferase gene reporter vector pmiRGLO (Promega).…”

“…The pmirGLO‐DLGAP1‐AS2‐WT or pmirGLO‐DLGAP1‐AS2‐MUT was co‐transfected into U2OS and Soas2 cells with miR‐451a mimics or NC mimics for 48 h, and then detected using the luciferase reporter assay system (Promega). 25 Similarly, wild‐type HK2 and mutant‐type HK2 were cloned into the firefly luciferase gene reporter vector pmiRGLO (Promega). The pmirGLO‐HK2‐WT or pmirGLO‐HK2‐MUT was co‐transfected with miR‐451a mimics, miR‐451a mimics plus DLGAP1‐AS2, or NC mimics into U2OS and Soas2 cells.…”

Comprehensive Analysis of Molecular Clusters and Prognostic Signature Based on m7G-related LncRNAs in Esophageal Squamous Cell Carcinoma

“…For example, Zhang (18) et al found that lncRNA SNHG7 was highly expressed in gastric cancer tissues and was closely associated with the proliferation, apoptosis, invasion and metastasis of gastric cancer cells. Among the 7 candidate lncRNAs, only HAND2-AS1 and SNHG7 had been reported as prognostic factors in ESCC (19,20); the rest of lncRNAs were identified as prognostic signatures in BC for the first time.…”

Crucial Roles of miR-625 in Human Cancer

“…In malignant pleural mesothelioma (MPM) (34,35) and thyroid cancer (TC) (36,37), miR-625 was found to be upregulated. It is downregulated in bladder cancer (38), nasopharyngeal carcinoma (NPC) (39), lung cancer (40)(41)(42)(43)(44)(45)(46), HCC (47), cervical cancer (CC) (48,49), osteosarcoma (50), melanoma (51)(52)(53)(54), laryngeal squamous cell carcinoma (LSCC) (55), acute myeloid leukemia (AML) (56), BC (57)(58)(59), glioma (60,61), esophageal cancer (EC) (62)(63)(64), clear cell renal cell carcinoma (65), GC (66)(67)(68)(69)(70), and pancreatic ductal adenocarcinoma (PDAC) (71). In colorectal cancer (CRC), the expression of miR-625 seems to vary, being either high or low.…”