&lt;p&gt;LncRNA SNHG6 Inhibits Apoptosis by Regulating EZH2 Expression via the Sponging of MiR-101-3p in Esophageal Squamous-Cell Carcinoma&lt;/p&gt;

Wang, Jiang; Yang, Xin; Li, Ruijia; Zhang, Rui; Hu, Desheng; Zhang, Yueli; Gao, Lei

doi:10.2147/ott.s275135

Cited by 15 publications

(18 citation statements)

References 28 publications

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“…The latest research showed that an inhibitor of EZH2 activity-GSK343 could significantly promote the differentiation of hematopoietic stem cells (HPCs) into MDSCs in the presence of granulocytemacrophage colony-stimulating factors (GM-CSF) and interleukin-6 (IL-6) in vitro [8]. In addition, the involvement of lncRNA Snhg6 in regulating EZH2 has also been reported [6,9]. So we speculate that lncRNA Snhg6 may regulate the differentiation of MDSCs through EZH2.…”

Section: To the Editormentioning

confidence: 85%

LncRNA Snhg6 regulates the differentiation of MDSCs by regulating the ubiquitination of EZH2

Lü

Cao²,

et al. 2021

J Hematol Oncol

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Myeloid-derived suppressor cells (MDSCs) are derived from bone marrow progenitor cells commonly, which is a heterogeneous cell group composed of immature granulocytes, dendritic cells, macrophages and early undifferentiated bone marrow precursor cells. Its differentiation and immunosuppressive function are regulated by complex network signals, but the specific regulation mechanisms are not yet fully understood. In this study, we found that in mouse of Lewis lung cancer xenograft, long non-coding RNA Snhg6 (lncRNA Snhg6) was highly expressed in tumor-derived MDSCs compared with spleen-derived MDSCs. LncRNA Snhg6 facilitated the differentiation of CD11b+ Ly6G− Ly6Chigh monocytic MDSCs (Mo-MDSCs) rather than CD11b+ Ly6G+ Ly6Clow polymorphonuclear MDSCs (PMN-MDSCs), but did not affect the immunosuppressive function of MDSCs. Notably, lncRNA Snhg6 could inhibit the expression of EZH2 by ubiquitination pathway at protein level rather than mRNA level during the differentiation of mouse bone marrow cells into MDSCs in vitro. EZH2 may be an important factor in the regulation of lncRNA Snhg6 to promote the differentiation of Mo-MDSCs. So what we found may provide new ideas and targets for anti-tumor immunotherapy targeting MDSCs.

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Section: To the Editormentioning

confidence: 85%

LncRNA Snhg6 regulates the differentiation of MDSCs by regulating the ubiquitination of EZH2

Lü

Cao²,

et al. 2021

J Hematol Oncol

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“…Our previous research also revealed that EZH2 was upregulated in samples afflicted by EC and EZH2 was confirmed as an oncogene in esophageal cancer via biological experiments (22). Recent studies have revealed that EZH2 promoted chemotherapeutic drug resistance in numerous cancers (23,24).…”

Section: Introductionmentioning

confidence: 88%

Melatonin sensitizes esophageal cancer cells to 5‑fluorouracil via promotion of apoptosis by regulating EZH2 expression

Zhang

Zhang²,

Li³

et al. 2021

Oncol Rep

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The present study aimed to investigate the effects of melatonin (MLT) and 5-fluorouracil (5-FU) combination on the chemotherapeutic effect of 5-FU in esophageal cancer, and determine the potential molecular mechanisms. The effects of MLT and 5-FU combination on cell proliferation, cell migration and invasion, and cell apoptosis were detected by Cell Counting Kit-8, Transwell assays and flow cytometric analysis, respectively. Quantitative PCR and western blotting were performed for mRNA and protein quantification, respectively. The present study revealed that MLT significantly inhibited cell activity in a dose-dependent manner and MLT significantly enhanced 5-FU-mediated inhibition of cell proliferation in esophageal cancer cells. Compared with the 5-FU group, the MLT and 5-FU combination group significantly inhibited the invasion and migration of EC-9706 and EC-109 cells. The present study also revealed that MLT and 5-FU synergistically promoted apoptosis via activation of the caspase-dependent apoptosis pathway. Histone-lysine N-methyltransferase EZH2 (EZH2) was highly expressed in esophageal cancer tissues and cells and its high expression promoted esophageal cancer progression. MLT and 5-FU combination inhibited cell proliferation and promoted apoptosis by regulating EZH2 expression. In conclusion, MLT enhanced 5-FU-mediated inhibition of cell proliferation via promotion of apoptosis by regulating EZH2 expression in esophageal cancer.

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“…Small nucleolar RNA host genes (SNHGs), for instance, play extremely important regulatory roles in ESCC. Specifically, lncRNA-SNHG6 can inhibit ESCC cell apoptosis by targeting miR-101-3p to regulate Enhancer of zeste homolog 2 (EZH2) (15). Furthermore, SNHG5 can inhibit the epithelial-mesenchymal transition process of ESCC cells through ubiquitination and degradation of metastasisassociated protein 2 (MTA2) (16).…”

Section: Discussionmentioning

confidence: 99%

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

Wang

Bao²,

Wan

et al. 2021

J Gastrointest Oncol

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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.

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<p>LncRNA SNHG6 Inhibits Apoptosis by Regulating EZH2 Expression via the Sponging of MiR-101-3p in Esophageal Squamous-Cell Carcinoma</p>

Cited by 15 publications

References 28 publications

LncRNA Snhg6 regulates the differentiation of MDSCs by regulating the ubiquitination of EZH2

LncRNA Snhg6 regulates the differentiation of MDSCs by regulating the ubiquitination of EZH2

Melatonin sensitizes esophageal cancer cells to 5‑fluorouracil via promotion of apoptosis by regulating EZH2 expression

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

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