Emerging Role of Non-Coding RNAs in Esophageal Squamous Cell Carcinoma

Feng, Qingqing; Zhang, Hongli; Yao, Denglin; Chen, Weidong; Wang, Yandong

doi:10.3390/ijms21010258

Cited by 62 publications

(58 citation statements)

References 152 publications

(150 reference statements)

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“…miRNAs play important regulatory roles in cell differentiation, proliferation, invasion, metastasis, and apoptosis (9). Currently, data are available on the miRNA signature of ESCC, and there are studies attempting to point out the potential value of miRNAs in ESCC screening, diagnosis, treatment, and prognosis (10). miR-216a-5p is a member of the miR-216 family (miR-216a/miR-216b), which has been shown to be dysregulated in several types of human cancers (11)(12)(13)(14)(15)(16).…”

Section: Microrna-216a-5p Suppresses Esophageal Squamous Cell Carcinomentioning

confidence: 99%

MicroRNA‑216a‑5p suppresses esophageal squamous cell carcinoma progression by targeting KIAA0101

Sun

Yan

et al. 2020

Oncol Rep

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The KIAA0101 protein (also referred to as NS5ATP9 or Paf15) is overexpressed in esophageal squamous cell carcinoma (ESCC) and is associated with disease progression and poor patient survival, but how KIAA0101 expression is regulated remains unknown. The relationship between tumor miR-216a-5p expression and prognosis in patients with ESCC was revealed by survival analyses. Quantitative reverse-transcriptase PCR and western blot analysis were used to evaluate miR-216a-5p and KIAA0101 expression in human ESCC tissues and cell lines. The targeting of KIAA0101 by miR-216a-5p was verified by dual-luciferase reporter assays. The EC9706 and TE1 cell lines were transfected with miR-216a-5p mimics and inhibitor, or KIAA0101-specific shRNA and KIAA0101-expressing plasmids, in order to evaluate the effect of manipulating miR-216a-5p and KIAA0101 expression on ESCC cell proliferation, cell cycle progression, migration, and invasion. miR-216a-5p was lowly expressed and inversely correlated with KIAA0101 protein expression in ESCC tissues and cell lines. Lower miR-216a-5p expression was associated with worse prognosis in patients with ESCC. miR-216a-5p negatively regulated KIAA0101 expression by directly targeting the 3'-untranslated region of the KIAA0101 mRNA. Overexpression of miR-216a-5p suppressed the proliferation, migration, and invasion of the ESCC cell lines, whereas inhibition of miR-216a-5p had the opposite effects. Meanwhile, KIAA0101 promoted ESCC migration and invasion, and its overexpression abolished the antitumor effects of miR-216a-5p mimics. As a tumor suppressor, miR-216a-5p targets KIAA0101 to inhibit the proliferation, migration, and invasion of ESCC. Therefore, the miR-216a-5p/KIAA0101 axis may be a potential target for ESCC treatment.

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Section: Microrna-216a-5p Suppresses Esophageal Squamous Cell Carcinomentioning

confidence: 99%

MicroRNA‑216a‑5p suppresses esophageal squamous cell carcinoma progression by targeting KIAA0101

Sun

Yan

et al. 2020

Oncol Rep

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“…Recent studies on lncRNAs have attracted increasing attention due to the involvement of these molecules in cancer oncogenesis and progression ( 38 - 40 ). Studies have reported the expression of hundreds of lncRNAs in ESCC, and differentially expressed lncRNAs have been shown to be closely related to ESCC malignancy through their effects on a wide range of tumor behaviors ( 41 , 42 ). Therefore, it is necessary to clarify the functions of lncRNAs in ESCC and thus identify effective diagnostic markers and treatment targets.…”

Section: Discussionmentioning

confidence: 99%

Long intergenic non‑coding RNA LINC01232 contributes to esophageal squamous cell carcinoma progression by sequestering microRNA‑654‑3p and consequently promoting hepatoma‑derived growth factor expression

et al. 2020

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Long intergenic non-coding RNA 01232 (LINC01232) was identified as a critical regulator of the development of pancreatic adenocarcinoma. The present study investigated the expression and regulatory roles of LINC01232 in esophageal squamous cell carcinoma (ESCC). The main aim of the present study was to elucidate the underlying mechanisms through which LINC01232 affects the malignancy of ESCC. Initially, LINC01232 expression in ESCC was analyzed using the TCGA and GTEx databases and was confirmed using reverse transcription-quantitative polymerase chain reaction. ESCC cell proliferation, apoptosis and migration and invasion were assessed using the Cell Counting kit-8 assay, flow cytometric analysis, and migration and invasion assays, respectively. ESCC tumor growth in vivo was examined using a xenograft mouse model. As shown by the results, a high LINC01232 expression was detected in ESCC tissues and cell lines. LINC01232 downregulation suppressed the proliferation, migration and invasion of ESCC cells, and promoted cell apoptosis in vitro . In addition, LINC01232 depletion restricted tumor growth in vivo . Mechanistically, LINC01232 was shown to function as an microRNA-654-3p (miR-654-3p) sponge in ESCC cells, and hepatoma-derived growth factor (HDGF) was identified as a direct target of miR-654-3p. LINC01232 could bind competitively to miR-654-3p and decrease its expression in ESCC cells, thereby promoting HDGF expression. Rescue experiments reconfirmed that the effects of LINC01232 deficiency in ESCC cells were restored by increasing the output of the miR-654-3p/HDGF axis. On the whole, the present study demonstrates that LINC01232 plays a tumor-promoting role during the progression of ESCC by regulating the miR-654-3p/HDGF axis. The LINC01232/miR-654-3p/HDGF pathway may thus provide a novel theoretical basis for the management of ESCC.

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“…The role of lncRNAs in ESCC formation and progression has gradually emerged [5]. LncRNA FAM83H-AS1 has been reported to play an oncogenic role in tumors by modulating cell proliferation, migration and invasion [11,[21][22][23][24].…”

Section: Discussionmentioning

confidence: 99%

“…Recently, increasing ndings support that long noncoding RNAs (lncRNAs) are crucial regulators in ESCC formation and progression [5][6][7][8][9][10]. Some lncRNAs modulate ESCC cell migration and invasion, and might be novel prognostic indicators, speci cally, biomarkers, for the early detection of metastasis in ESCC [5,9]. For instance, lncRNA DLX6 antisense RNA 1 (DLX6-AS1) expression was signi cantly increased in ESCC tissues, and DLX6-AS1 knockdown inhibited ESCC cell proliferation, migration and invasion [6].…”

Section: Introductionmentioning

confidence: 99%

LncRNA FAM83H-AS1 Promotes Aerobic Glycolysis and Tumor Progression by Regulating miR-4684-5p/ZBTB38 Axis in Esophageal Squamous Cell Carcinoma

Qian

Chen

et al. 2020

Preprint

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Background: Dysregulation of lncRNAs is implicated in esophageal squamous cell carcinoma (ESCC) progression; However, the precise function of lncRNA FAM83H-AS1 in ESCC remains unknown. Methods: FAM83H-AS1, miR-4684-5p and ZBTB38 mRNA expressions were detected via qRT-PCR. ZBTB38, GLUT1 and LDH-A protein expressions were tested via Western blot. Cell proliferation, migration and invasion were evaluated via CCK-8 and transwell assay, respectively. A nude mouse xenograft model was used to investigate the role of FAM83H-AS1 in xenograft ESCC growth. The metabolic shift in ESCC cells was examined via glycolysis analysis. The interaction between FAM83H-AS1, miR-4684-5p and ZBTB38 was analyzed via computational algorithms, RNA pull-down, RIP and dual luciferase reporter assay. Results: We found that FAM83H-AS1 was upmodulated in ESCC cell lines. FAM83H-AS1 knockdown hampered ESCC cell proliferation, migration, invasion and aerobic glycolysis, while FAM83H-AS1 overexpression demonstrated the opposite effects. FAM83H-AS1 knockdown also delayed the tumor growth in vivo. Moreover, FAM83H-AS1 interacted with miR-4684-5p/ZBTB38 axis in ESCC cells. ZBTB38 overexpression or miR-4684-5p inhibition partially reversed the inhibitory effect of FAM83H-AS1 knockdown on cell migration, invasion and aerobic glycolysis in ESCC cells. Conclusion: Our present results indicate FAM83H-AS1 accelerated aerobic glycolysis and tumorigenesis of ESCC by sponging miR-4684-5p and triggering the expression of ZBTB38, providing new insights into mechanism of ESCC progression and therapeutic strategy.

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Emerging Role of Non-Coding RNAs in Esophageal Squamous Cell Carcinoma

Cited by 62 publications

References 152 publications

MicroRNA‑216a‑5p suppresses esophageal squamous cell carcinoma progression by targeting KIAA0101

MicroRNA‑216a‑5p suppresses esophageal squamous cell carcinoma progression by targeting KIAA0101

Long intergenic non‑coding RNA LINC01232 contributes to esophageal squamous cell carcinoma progression by sequestering microRNA‑654‑3p and consequently promoting hepatoma‑derived growth factor expression

LncRNA FAM83H-AS1 Promotes Aerobic Glycolysis and Tumor Progression by Regulating miR-4684-5p/ZBTB38 Axis in Esophageal Squamous Cell Carcinoma

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