&lt;p&gt;LncRNA SNHG1 Regulates the Progression of Esophageal Squamous Cell Cancer by the miR-204/HOXC8 Axis&lt;/p&gt;

Li, Hao Miao; Yu, Yongjun; Liu, Qi; Wei, Xiu Feng; Zhang, Jun; Zhang, Rui Xiang; Sun, Hai; Wang, Zong Fei; Xing, Wen Qun; Li, Yin

doi:10.2147/ott.s224550

Cited by 20 publications

(14 citation statements)

References 35 publications

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“…It is well-recognized that lncRNAs may function as endogenous sponges to regulate miRNA function in diseases [26]. For example, a prior research displayed that SNHG1 could bind to miR-204 to inhibit it, thus promoting migratory, and invasive abilities but repressing apoptosis in esophageal squamous cell cancer [27]. These ndings indirectly con rmed the binding relationship between SNHG1 and miR-9-3p in bladder cancer cells which observed by our study.…”

Section: Discussionsupporting

confidence: 86%

The Oncogenic Capacities of Long Noncoding RNA SNHG1 in Bladder Cancer by inducing proliferation and repressing apoptosis via upregulation of microRNA-9-3p-targeted MDM2

et al. 2021

Preprint

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Background The involvement of long noncoding RNA small nucleolar RNA host gene 1 (lncRNA SNHG1) was documented in numerous cancers, including bladder, pancreatic and prostate cancers. However, the further mechanistic investigation of SNHG1 in bladder is still needed to conduct. With this purpose, tissue, cell, and animal experiments were implemented in our research to figure out the specific mechanism of SNHG1 in bladder cancer via microRNA-9-3p (miR-9-3p). Methods In harvested bladder cancer tissues, RNA-FISH and RT-qPCR were adopted for SNHG1 expression measurement and RT-qPCR for miR-9-3p expression determination. The impacts of SNHG1, miR-9-3p, MDM2, and PPARγ on cell viability, proliferation, and apoptosis were evaluated by gain- and loss-of-function approaches. RT-qPCR and western blot analysis were performed to detect expression of MDM2, PPARγ, and apoptosis-related factors. RNA pull-down, RIP, dual luciferase reporter gene assay, and IP experiment were utilized to assess the modulatory relationship among SNHG1, miR-9-3p, MDM2, and PPARγ. Tumorigenic ability of bladder cancer cells was measured in vivo. Results High SNHG1 and poor miR-9-3p expression was identified in bladder cancer tissues and cells. Mechanistically, SNHG1 bound to miR-9-3p which negatively targeted MDM2. MDM2 augmented PPARγ ubiquitination to downregulate PPARγ. Bladder cancer cell proliferation was diminished and cell apoptosis was enhanced by silencing SNHG1 or MDM2 or overexpressing miR-9-3p. Similarly, SNHG1 silencing orchestrated miR-9-3p/MDM2/PPARγ axis to depress bladder cancer cell tumorigenesis in vivo. Conclusion In summary, the obtained data provided the novel insight of the anti-oncogenic mechanism of silencing SNHG1 in bladder cancer by activating PPARγ via downregulation of miR-9-3p-targeted MDM2.

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Section: Discussionsupporting

confidence: 86%

The Oncogenic Capacities of Long Noncoding RNA SNHG1 in Bladder Cancer by inducing proliferation and repressing apoptosis via upregulation of microRNA-9-3p-targeted MDM2

et al. 2021

Preprint

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“…Nrf-2 is a pleiotropic protein that inhibits the transcriptional activation of its downstream target NF- κ B by acting on antioxidant response elements and ultimately regulates the expression of a series of antioxidants and other genes [ 12 ]. Recent studies have shown that [ 13 , 14 ] miR-204 is a new regulator of innate immune response, which can significantly improve the survival rate of LPS-induced sepsis by preventing NF- κ B-mediated inflammation. This study established an acute lung injury model induced by lipopolysaccharide and explored the specific mechanism of miR-204 in lung injury induced by lipopolysaccharide and the specific mechanism of HA.…”

Section: Introductionmentioning

confidence: 99%

Mir-204 Regulates LPS-Induced A549 Cell Damage by Targeting FOXK2

Zhao

et al. 2021

Journal of Healthcare Engineering

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Objective. To assess whether miR-204 and HA affect A549 cell injury induced by lipopolysaccharide. Material and Methods. A549 cells were treated with hirsutanol A, and cell damage was induced by LPS followed by analysis of cell proliferation by CCK-8, cell apoptosis by flow cytometry, apoptosis-related protein expression by western blot, downstream target of miR-20 by dual-luciferase reporter gene, and inflammatory factors by ELISA and PCR. Results. LPS can significantly inhibit the viability of A549 cells, induce cell apoptosis, and promote the release of IL-6, IL-1β, and TNF-α, while HA pretreatment can target FOXK2 by upregulating miR-204 levels, thereby alleviating apoptosis and promoting cell viability and at the same time inhibiting the release of inflammatory factors by inhibiting the activation of NF-κB. Conclusions. miR-204 participates in the protection of HA acute lung injury by targeting FOXK2.

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“…In EC, various lncRNAs have been suggested to regulate cellular biology. It is recently known that suppression of lncRNA gradually increased during hepatocarcinogenesis delays the progression of EC via the ceRNA network [ 9 ], and the same regulatory mechanism has been observed in small nucleolar RNA host gene 1-regulated EC progression [ 10 ]. Long non-coding RNA 00114 (LINC00114) has been indicated to stimulate the progression and radioresistance of nasopharyngeal carcinoma (NPC) [ 11 ].…”

Section: Introductionmentioning

confidence: 99%

LINC00114 stimulates growth and glycolysis of esophageal cancer cells by recruiting EZH2 to enhance H3K27me3 of DLC1

Qin

et al. 2022

Clin Epigenet

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Objective LINC00114 could promote the development of colorectal cancer, but its mechanism has been rarely discussed in esophageal cancer (EC). Herein, we explored the molecular mechanism of LINC00114 via mediating enhancer of zeste homolog 2/deleted in liver cancer 1 (EZH2/DLC1) axis in EC. Methods LINC00114, EZH2 and DLC1 expression in EC tissues and cells were tested. LINC00114, EZH2 and DLC1 expression were altered in EC cells through transfection with different constructs, and cell proliferation, migration, invasion, apoptosis and glycolysis were subsequently observed. The interaction between LINC00114 and EZH2 and that between EZH2 and DLC1 were explored. Tumor formation was also conducted to confirm the in vitro results. Results The expression levels of LINC00114 and EZH2 were elevated while those of DLC1 were reduced in EC. Inhibiting LINC00114 or reducing EZH2 blocked cell proliferation, migration, invasion and glycolysis and induce cell apoptosis in EC. LINC00114 promoted H3K27 trimethylation of DLC1 by recruiting EZH2. Knockdown of DLC1 stimulated cell growth and glycolysis in EC and even mitigated the role of LINC00114 inhibition in EC. In vivo experiment further confirmed the anti-tumor effect of LINC00114 inhibition in EC. Conclusion The data indicate that LINC00114 promotes the development of EC by recruiting EZH2 to enhance H3K27me3 of DLC1.

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<p>LncRNA SNHG1 Regulates the Progression of Esophageal Squamous Cell Cancer by the miR-204/HOXC8 Axis</p>

Cited by 20 publications

References 35 publications

The Oncogenic Capacities of Long Noncoding RNA SNHG1 in Bladder Cancer by inducing proliferation and repressing apoptosis via upregulation of microRNA-9-3p-targeted MDM2

The Oncogenic Capacities of Long Noncoding RNA SNHG1 in Bladder Cancer by inducing proliferation and repressing apoptosis via upregulation of microRNA-9-3p-targeted MDM2

Mir-204 Regulates LPS-Induced A549 Cell Damage by Targeting FOXK2

LINC00114 stimulates growth and glycolysis of esophageal cancer cells by recruiting EZH2 to enhance H3K27me3 of DLC1

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