&lt;p&gt;Exosomes-Derived Long Non-Coding RNA HOTAIR Reduces Laryngeal Cancer Radiosensitivity by Regulating microRNA-454-3p/E2F2 Axis&lt;/p&gt;

Cui, Xiangyan; Dong, Xiao; Wang, Xin

doi:10.2147/ott.s224881

Cited by 25 publications

(19 citation statements)

References 31 publications

(35 reference statements)

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“…In this study, LINC00261 was mainly located in the cytoplasm of ESCC cells by subcellular separation assay, illustrating that LINC00261 might modulate its downstream gene expression after transcription. Bioinformatics websites predicted the target gene of LINC00261 and identified miR-545-3p which has been reported to exert major roles in multiples cancers, such as non-small-cell lung cancer cells , hepatocellular carcinoma (Changjun et al, 2018), and laryngeal cancer (Cui et al, 2019). Our present study verified that LINC00261 served as a ceRNA for miR-545-3p and negatively regulated miR-545-3p expression.…”

Section: Discussionsupporting

confidence: 76%

LINC00261 Suppresses Cisplatin Resistance of Esophageal Squamous Cell Carcinoma Through miR-545-3p/MT1M Axis

Wang

Liu

et al. 2021

Front. Cell Dev. Biol.

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To improve the survival rate and cure rate of patients, it is necessary to find a new treatment scheme according to the molecular composition of (ESCC) in esophageal squamous cell carcinoma. Long non-coding RNAs (lncRNAs) regulate the progression of ESCC by various pathophysiological pathways. We explored the possible function of the lncRNA LINC00261 (LINC00261) on cisplatin (DDP) resistance of ESCC and its relative molecular mechanisms. In the study, we found that LINC00261 was downregulated in ESCC tissues, cell lines, and DDP-resistant ESCC patients. Besides, overexpression of LINC00261 not only inhibited cell proliferation, and DDP resistance but also promotes cell apoptosis. Further mechanistic research showed that LINC00261 sponged miR-545-3p which was negatively correlated with the expression of LINC00261. In addition, functional experiments revealed that upregulation of miR-766-5p promoted proliferation and enhanced DDP resistance. Subsequently, MT1M was testified to be the downstream target gene of miR-545-3p. Rescue experiments revealed that overexpression of MT1M largely restores miR-545-3p mimics-mediated function on ESCC progression. Our results demonstrate that the LINC00261 suppressed the DDP resistance of ESCC through miR-545-3p/MT1M axis.

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Section: Discussionsupporting

confidence: 76%

LINC00261 Suppresses Cisplatin Resistance of Esophageal Squamous Cell Carcinoma Through miR-545-3p/MT1M Axis

Wang

Liu

et al. 2021

Front. Cell Dev. Biol.

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“…The cells were observed under a dissecting light microscope (magnification, ×100), and the colonies containing >50 cells were counted. The survival fraction (SF) were calculated as follows: SF = (number of colonies/number of cells plated) irradiated /(number of colonies/number of cells plated) non-irradiated ( 30 ) The SF in each group was also analyzed using GraphPad Prism 5.0 (GraphPad Software, Inc.) as previously described ( 31 ).…”

Section: Methodsmentioning

confidence: 99%

miR‑7/SP1/TP53BP1 axis may play a pivotal role in NSCLC radiosensitivity

et al. 2020

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MicroRNA-7 (miR-7) has been identified as a tumor suppressor in non-small cell lung cancer (NSCLC) and a radiosensitivity regulator. Numerous studies have revealed that specific protein 1 (SP1) plays a critical role in the tumorigenesis of various types of cancers and regulates radiosensitivity and tumor suppressor p53-binding protein 1 (TP53BP1), which plays an essential role in DNA repair. However, it is not clear whether miR-7 has a regulatory effect on SP1 and TP53BP1 in NSCLC. In the present study it was revealed that miR-7 directly binds to the 3′UTR of SP1, thereby suppressing SP1 expression to regulate radiosensitivity. Overexpression of miR-7 and SP1 and knockdown of miR-7 and SP1 were performed using lentiviral transfection. Protein and mRNA abundance of SP1 and TP53BP1 were determined using western blotting and RT-qPCR, respectively, while miR-7 binding to SP1 was validated using a luciferase reporter assay. Biological function analysis indicated that miR-7 negatively regulated SP1 and inhibited cell proliferation, migration, and invasion when combined with radiation. It was also revealed that the expression of TP53BP1 was positively regulated by SP1 or negatively regulated by miR-7. In conclusion, SP1 was a target of miR-7, and the decreased expression of SP1 resulting from miR-7 overexpression in NSCLC was vital for improving radiosensitivity in NSCLC cells. Moreover, SP1 expression was detected in 95 paired NSCLC and adjacent normal tissues, and it was determined that SP1 was significantly upregulated in NSCLC tissues and that its upregulation was correlated with the degree of tissue differentiation. Thus, SP1 and/or miR-7 may be potential molecular targets in NSCLC radiotherapy.

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“…microRNAs are involved in multiple biological processes, including cellular differentiation, proliferation, and apoptosis 34,35 . Previous studies have demonstrated that miR‐545‐3p affects the pathogenesis of various cancers 36–38 . miR‐545‐3p was shown to be elevated in H/R‐induced H9C2 cells and the overexpression of miR‐545‐3p significantly down‐regulated the apoptosis of H9C2 cells.…”

Section: Discussionmentioning

confidence: 99%

lncRNA XIST knockdown suppresses hypoxia/reoxygenation (H/R)‐induced apoptosis of H9C2 cells by regulating miR‐545‐3p/G3BP2

Xiao

Tong

et al. 2021

IUBMB Life

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This study was aimed at determining the roles and functions of lncRNA XIST/miR‐545‐3p/G3BP2 axis during hypoxia/reoxygenation (H/R)‐induced H9C2 cell apoptosis. H9C2 cells were distributed into two groups, the H/R injury and control groups. High‐throughput lncRNA sequencing was applied in the determination of differentially expressed lncRNAs between H/R‐induced H9C2 cells and normal H9C2 cells. Real‐time polymerase chain reactions (RT‐PCR) were used to confirm the expression levels of lncRNA XIST in H/R‐induced H9C2 cells. H9C2 cells were then transfected with lncRNA XIST recombinant plasmid (lncRNA XIST), sh‐LINC XIST, agomiR‐545‐3p, antagomiR‐545‐3p, pcDNA‐G3BP2, sh‐G3BP2, and a corresponding negative control (NC). Bioinformatic analyses revealed that MiR‐545‐3p was a target for lncRNA XIST. This finding was confirmed by dual‐luciferase reporter assay. The degree of cell apoptosis was evaluated by a flow cytometer. RT‐PCR and western blot were performed to assess the apoptotic‐related proteins in each group. A total of 859 differentially expressed lncRNAs (up‐regulated = 502, down‐regulated = 357) were identified. LncRNA XIST was found to be down‐regulated in H/R‐induced H9C2 cells while miR‐545‐3p was distinctly up‐regulated. miR‐545‐3p was established to be a direct target for LncRNA XIST. LncRNA XIST significantly enhanced the apoptotic rate, while its inhibition suppressed the apoptotic rate. AgomiR‐545‐3p partially blocked the lncRNA XIST and enhanced the apoptosis of H/R‐induced H9C2 cells. Moreover, miR‐545‐3p was shown to be a direct target for G3BP2. The overexpression of G3BP2 partially reversed the apoptotic effects of miR‐545‐3p on H/R‐induced H9C2 cells. lncRNA XIST/miR‐545‐3p/GBP2 was found to be an apoptotic regulator in H/R‐induced H9C2 cells.

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<p>Exosomes-Derived Long Non-Coding RNA HOTAIR Reduces Laryngeal Cancer Radiosensitivity by Regulating microRNA-454-3p/E2F2 Axis</p>

Cited by 25 publications

References 31 publications

LINC00261 Suppresses Cisplatin Resistance of Esophageal Squamous Cell Carcinoma Through miR-545-3p/MT1M Axis

LINC00261 Suppresses Cisplatin Resistance of Esophageal Squamous Cell Carcinoma Through miR-545-3p/MT1M Axis

miR‑7/SP1/TP53BP1 axis may play a pivotal role in NSCLC radiosensitivity

lncRNA XIST knockdown suppresses hypoxia/reoxygenation (H/R)‐induced apoptosis of H9C2 cells by regulating miR‐545‐3p/G3BP2

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