LncRNA SNHG6 enhances the radioresistance and promotes the growth of cervical cancer cells by sponging miR-485-3p

Liu, Jin; Liu, Xiaojiao; Li, Rong

doi:10.1186/s12935-020-01448-9

Cited by 24 publications

(20 citation statements)

References 31 publications

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“…[9][10][11] Furthermore, accumulating evidence pointed out that SNHG6 was involved in drug resistance and radio-resistance. 12 SNHG6 was reported to promote the 5-fluorouracil resistance in colorectal cancer by regulating miR-26a-5p. 13 Also, SNHG6 sponges miR-485-3p to enhance radio-resistance.…”

Section: Introductionmentioning

confidence: 99%

“… 13 Also, SNHG6 sponges miR-485-3p to enhance radio-resistance. 12 Thus, it can be inferred that SNHG6 regulate 5-fluorouracil resistance and radio-resistance through mediating DNA damage response pathway, which is the main cause for cisplatin resistance as well. Besides, Cao et al reported that SNHG6 enhanced paclitaxel resistance as well, indicating its potential role in regulating the cell cycle.…”

Section: Introductionmentioning

confidence: 99%

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<p>SNHG6 Interacted with miR-325-3p to Regulate Cisplatin Resistance of Gastric Cancer by Targeting GITR</p>

Sun¹,

Li²,

Zhu³

et al. 2020

OTT

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Background: Cisplatin resistance results in the failure of platinum-based chemotherapy and relapse of gastric cancer. We aimed to investigate the potential regulating role of SNHG6/ miR-325-3p/GITR in reversing cisplatin resistance. Patients and Methods: A total of 137 gastric cancer patients were recruited. qRT-PCR and ELISA were used to test the expression of target genes. CCK-8 and caspase 3/7 kit were used to test the cell viability and apoptosis rate. Dual luciferase reporter gene and RNA-pull down assay were used to investigate the potential interaction between target genes. Results: SNHG6 and GITR were up regulated in gastric cancer; however, miR-325-3p was down-regulated. Besides, SNHG6, miR-325-3p and GITR expression were associated with gastric cancer prognosis. Then, we found that GITR and SNHG6 promoted proliferation and inhibited apoptosis of MKN45 and MKN45 cisplatin resistance cell line; however, miR-325-3p inhibited proliferation and promoted apoptosis of these cell lines. Furthermore, SNHG6 might bind to miR-325-3p to regulate its expression, and miR-325-3p directly interacted with the 3`UTR of GITR. Conclusion: SNHG6 binds to miR-325-3p, which directly interacted with GITR to regulate cisplatin resistance of gastric cancer.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

<p>SNHG6 Interacted with miR-325-3p to Regulate Cisplatin Resistance of Gastric Cancer by Targeting GITR</p>

Sun¹,

Li²,

Zhu³

et al. 2020

OTT

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“…SNHG6 upregulation is associated with poor prognosis of patients with colorectal cancer [ 273 ]. SNHG6 can also enhance radio-resistance of cervical cancer cells [ 274 ]. In colorectal cancer cells, SNHG6 overexpression occurs due to SP1 stimulation and DNA copy number gains.…”

Section: Non-coding Rnas and Ezh2 Signalingmentioning

confidence: 99%

“…Importantly, lncRNAs can affects EMT via EZH2 regulation. The lncRNA H19 is a tumor-promoting factor capable of enhancing cancer proliferation and invasion via p53 down-regulation and subsequent induction of TNFAIP8 [ 274 ]. Silencing H19 is in favor of apoptosis induction and impairing breast cancer proliferation [ 296 ].…”

Section: Non-coding Rnas and Ezh2 Signalingmentioning

confidence: 99%

The long and short non-coding RNAs modulating EZH2 signaling in cancer

et al. 2022

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Non-coding RNAs (ncRNAs) are a large family of RNA molecules with no capability in encoding proteins. However, they participate in developmental and biological processes and their abnormal expression affects cancer progression. These RNA molecules can function as upstream mediators of different signaling pathways and enhancer of zeste homolog 2 (EZH2) is among them. Briefly, EZH2 belongs to PRCs family and can exert functional roles in cells due to its methyltransferase activity. EZH2 affects gene expression via inducing H3K27me3. In the present review, our aim is to provide a mechanistic discussion of ncRNAs role in regulating EZH2 expression in different cancers. MiRNAs can dually induce/inhibit EZH2 in cancer cells to affect downstream targets such as Wnt, STAT3 and EMT. Furthermore, miRNAs can regulate therapy response of cancer cells via affecting EZH2 signaling. It is noteworthy that EZH2 can reduce miRNA expression by binding to promoter and exerting its methyltransferase activity. Small-interfering RNA (siRNA) and short-hairpin RNA (shRNA) are synthetic, short ncRNAs capable of reducing EZH2 expression and suppressing cancer progression. LncRNAs mainly regulate EZH2 expression via targeting miRNAs. Furthermore, lncRNAs induce EZH2 by modulating miRNA expression. Circular RNAs (CircRNAs), like lncRNAs, affect EZH2 expression via targeting miRNAs. These areas are discussed in the present review with a focus on molecular pathways leading to clinical translation.

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“…Importantly, the downregulation of miR-485-3p was found in glioblastoma patients, suggesting a promising prognostic target for glioblastoma (Wang, Zhang et al, 2017). Similarly, the cancer-inhibitory role of miR-485-3p was evidenced in breast cancer (Lou, Xiao et al, 2016), renal cancer (Lai, Xin et al, 2020), and cervical cancer (Liu, Liu et al, 2020). However, the association relationships between circ-KRT6C and miR-485-3p have not been fully elucidated yet in colorectal cancer.…”

Section: Introductionmentioning

confidence: 99%

circ-Keratin 6c Promotes Malignant Progression and Immune Evasion of Colorectal Cancer through microRNA-485-3p/Programmed Cell Death Receptor Ligand 1 Axis

Jiang

Hou

Liu

et al. 2021

J Pharmacol Exp Ther

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Background: Recently, circular RNA (circRNA) was reported to be a significant participant in the development of tumorigenesis, including colorectal cancer. Therefore, we aimed to clarify the precise role of circ-keratin 6C (circ-KRT6C) in colorectal cancer progression. Methods: The relative expression levels of circ-KRT6C, microRNA-16-5p (miR-485-3p), and programmed cell death receptor ligand 1 (PDL1) were analyzed by real-time quantitative polymerase chain reaction and western blot assays. The proliferation was assessed by cell count kit 8 and colony-forming assays. The apoptotic cells were determined by flow cytometry assay. The migration and invasion were analyzed by transwell assay. Colorectal cancer cells were co-cultured with peripheral blood mononuclear cells or cytokine-induced killer cells to assess immune response. The interaction relationships among circ-KRT6C, miR-485-3p, and PDL1 were examined by dual-luciferase reporter assay. The effects of circ-KRT6C inhibition in vivo was analyzed by an animal experiment. Results: Circ-KRT6C was overexpressed in colorectal cancer tissues and cells, and its level was associated with overall survival time of colorectal cancer patients. The suppression of circ-KRT6C suppressed growth, migration, invasion, and immune escape while stimulated apoptosis in colorectal cancer cells, which was abolished by shortage of miR-485-3p. In addition, overexpression of miR-485-3p repressed malignant progression and immune evasion of colorectal cancer by targeting PDL1, implying that PDL1 was a functional target of miR-485-3p. A xenograft experiment also suggested that circ-KRT6C inhibition could repress tumor growth in vivo. Conclusion: Circ-KRT6C could increase PDL1 expression by functioning as a miR-485-3p sponge, which promoted malignant progression and immune evasion of colorectal cancer cells.

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LncRNA SNHG6 enhances the radioresistance and promotes the growth of cervical cancer cells by sponging miR-485-3p

Cited by 24 publications

References 31 publications

<p>SNHG6 Interacted with miR-325-3p to Regulate Cisplatin Resistance of Gastric Cancer by Targeting GITR</p>

<p>SNHG6 Interacted with miR-325-3p to Regulate Cisplatin Resistance of Gastric Cancer by Targeting GITR</p>

The long and short non-coding RNAs modulating EZH2 signaling in cancer

circ-Keratin 6c Promotes Malignant Progression and Immune Evasion of Colorectal Cancer through microRNA-485-3p/Programmed Cell Death Receptor Ligand 1 Axis

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