&lt;p&gt;LncRNA LINC01116 Promotes Cancer Cell Proliferation, Migration And Invasion In Gastric Cancer By Positively Interacting With lncRNA CASC11&lt;/p&gt;

Su, Xiaohui; Zhang, Jianjun; Luo, Xin; Yang, Wei; Liu, Yanqing; Liu, Yang; Shan, Zexing

doi:10.2147/ott.s208133

Cited by 19 publications

(19 citation statements)

References 18 publications

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“…LncRNA LINC01116 has been shown to play an oncogenic role in multiple human cancers. [17][18][19][20][21] qPCR assay detected up-regulation of LINC01116 expression in prostate cancer cells as compared to that in normal human prostate epithelial cells, which encouraged the subsequent functional assays. 16 siRNA-induced knockdown of LINC01116 decreased prostate cancer cell proliferation, and the disruption of the LINC01116 gene with a CRISPR/CAS9 system resulted in a four-fold reduction in the number of prostate cancer cell colony formation, which supporting the oncogenic role of LINC01116 in prostate cancer.…”

Section: Discussionmentioning

confidence: 99%

“…In addition, LINC01116 was reported to overexpressed and contributed to the progression of nasopharyngeal carcinoma, gastric cancer, osteosarcoma, glioma, epithelial ovarian cancer and head and neck squamous cell carcinoma. [17][18][19][20][21][22][23] However, there is little knowledge on the role of LINC01116 in NSCLC.…”

Section: Discussionmentioning

confidence: 99%

“…23 In addition, LINC01116 was identified to regulates tumorigenesis of glioma by targeting vascular endothelial growth factor A (VEGFA), 22 and LINC01116 was shown to promote gastric cancer cell invasion and migration by positively interacting with lncRNA CASC11. 20 A recent study showed that LINC01116 contributed to gefitinib resistance in NSCLC cells by regulating IFI44 expression. 24 However, the mechanism underlying the contribution of LINC01116 to cisplatin resistance remains unknown in NSCLC until now.…”

Section: Discussionmentioning

confidence: 99%

“…17,18 Previous studies have also demonstrated that LINC01116 promotes the progression of nasopharyngeal carcinoma, gastric cancer, osteosarcoma, glioma and epithelial ovarian cancer. [19][20][21][22][23] Furthermore, a recent study showed LINC01116 contributed to gefitinib resistance in NSCLC through affecting IFI44 expression. 24 However, the involvement of LINC01116 in chemoresistance of LAD remains unknown until now.…”

Section: Introductionmentioning

confidence: 99%

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<p>LncRNA LINC01116 Contributes to Cisplatin Resistance in Lung Adenocarcinoma</p>

Wang¹,

Gao²,

Chen³

et al. 2020

OTT

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Background: Long non-coding RNAs (lncRNAs) have been found to contribute to cisplatin resistance in several cancers; however, the role of lncRNA LINC01116 in cisplatin resistance remains unknown in non-small-cell lung cancer. This study aimed to examine the contribution of LINC01116 to cisplatin resistance in lung adenocarcinoma (LAD). Materials and Methods: Cisplatin-resistant A549/DDP cells were generated by treatment with cisplatin by dose escalation. LINC01116 expression was compared between A549 and A549/DDP cells, and between cisplatin-resistant and non-resistant LAD specimens. The cell viability, colony formation, proliferation, migration and invasion were measured using MTT and Transwell assays, and cell apoptosis and cell cycle were detected using flow cytometry. The expression of E-cadherin and Vimentin was quantified. LAD xenografts were modeled in nude mice to investigate the role of LINC01116 on the resistance of LAD to cisplatin. Results: MTT assay measured the IC 50 values of 13.49 ± 1.62 and 3.52 ± 1.33 μg/mL for A549/DDP and A549 cells, respectively. LINC01116 was overexpressed in cisplatin-resistant LAD specimens and A549/DDP cells (P < 0.05). Knockdown of LINC01116 inhibited cell viability, proliferation, migration and invasion, promoted apoptosis and enhanced the sensitivity to cisplatin in A549/DDP cells, while LINC01116 overexpression promoted cell viability, proliferation, migration and invasion, inhibited apoptosis and reduced the sensitivity to cisplatin in A549 cells. LINC01116 knockdown resulted in a 2.1-fold increase in E-cadherin expression and a 56% reduction in Vimentin expression in A549/DDP cells, and LINC01116 overexpression resulted in a 45% reduction in E-cadherin expression and a 1.82fold increase in Vimentin expression in A549 cells. Conclusion: Dysregulation of lncRNA LINC01116 expression results in resistance of LAD to cisplatin via the EMT process. Our findings support the oncogenic role of LINC01116 to promote the development of cisplatin resistance in LAD, and LINC01116 may be a novel predictor of poor response to cisplatin.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

<p>LncRNA LINC01116 Contributes to Cisplatin Resistance in Lung Adenocarcinoma</p>

Wang¹,

Gao²,

Chen³

et al. 2020

OTT

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“…More and more studies showed that lncRNAs were involved in chromosome regulation, transcription and post-transcriptional regulation [4][5]. It has also been observed to be involved in the development and progression of other cancers, such as gastric cancer and liver cancer [6][7]. Several prognostic biomarkers for LUAD have been reported such as lncRNA LOC100132354 [8]and lncRNA CTB-193M12.5 [9], etc.…”

Section: Introductionmentioning

confidence: 99%

Six-long Non-coding RNA Signature to Predict the Prognosis of Lung Adenocarcinoma

Wang¹

2020

Preprint

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Background: Long non-coding RNAs (lncRNAs) have been reported to play essential roles in tumorigenesis and cancers prognosis, and they can be a potential cancer prognostic markers. However, in lung adenocarcinoma(LUAD), how lncRNA signatures predict the survival of patients is poorly understood. Our study aims to explore lncRNA signatures and prognostic function in LUAD.Methods: The expression and prognosis data of lncRNAs in LUAD patients was collected from the Cancer Genome Atlas (TCGA) data. All analyses were performed using the R package (version 3.6.2). Metascape, STRING and Cytoscape were used for enrichment analysis and function prediction of the lncRNA co-expressed protein-coding genes.Results: We have collected lncRNA expression data in 466 LUAD tumors, and a six-lncRNA signature(RP11-79H23.3, RP11-309M7.1, CTD-2357A8.3, RP11-108P20.4, U47924.29, LHFPL3-AS2) has been shown to be significantly related to LUAD patients’ overall survival. According to the lncRNA signatures, the high-risk and low-risk groups were divided in LUAD patients with different survival rates. Further multivariable cox regression analysis showed that the prognostic value of this signature was independent of clinical factors. The potential functional roles and hub co-expressed protein-coding genes in the six prognostic lncRNAs are shown in the functional enrichment analysis.Conclusions: These results showed that these six lncRNAs could be independent predicted prognostic biomarkers in LUAD patients.

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Hypoxia‐induced factor‐1α promotes radioresistance of esophageal cancer cells by transcriptionally activating LINC01116 and suppressing miR‐3612 under hypoxia

Zhang,

Wang,

et al. 2023

J Biochem & Molecular Tox

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Esophageal cancer (EC) is a challenging tumor to treat with radiotherapy, often exhibiting resistance to this treatment modality. To explore the factors influencing radioresistance, we focused on the role of hypoxia‐induced factor‐1α (HIF‐1α), and its interaction with the long noncoding RNA long intergenic nonprotein coding RNA 1116 (LINC01116). We analyzed the LINC01116 expression in EC and EC cell lines/human normal esophageal epithelial cell line (Het‐1A). LINC01116 was silenced/overexpressed in EC109/KYSE30 cells under hypoxia, followed by radioresistance assessment. We measured HIF‐1α levels in hypoxic EC cells and further validated the binding of HIF‐1α with LINC01116, analyzing their interaction in EC cells. We then performed experiments in EC109 cells by transfection them with sh‐HIF‐1α/oe‐LINC01116 to verify the effects. Additonally, we analyzed the localization of LINC01116 and its binding with miR‐3612, followed by a combined experiment performed to validate the results. Our findings indicated that LINC01116 was highly expressed in EC and further elevated in hypoxic EC cells. LINC01116 was expressed at a high level in EC, which was further elevated in EC cells under hypoxic conditions. Knockdown of LINC01116 triggered EC cell apoptosis, thus suppressing radioresistance. Further investigation revealed that HIF‐1α transcriptionally activated LINC01116 expression under hypoxia, and silencing HIF‐1α lowered EC cell radioresistance by downregulating LINC01116. Under hypoxic conditions, LINC01116 could function as a sponge for miR‐3612 and inhibit its expression. This interaction between LINC01116 and miR‐3612 played a crucial role in mediating radioresistance in EC cells. Briefly, under hypoxic conditions, HIF‐1α facilitates radioresistance of EC cells by transcriptionally activating LINC01116 expression and downregulating miR‐3612.

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<p>LncRNA LINC01116 Promotes Cancer Cell Proliferation, Migration And Invasion In Gastric Cancer By Positively Interacting With lncRNA CASC11</p>

Cited by 19 publications

References 18 publications

<p>LncRNA LINC01116 Contributes to Cisplatin Resistance in Lung Adenocarcinoma</p>

<p>LncRNA LINC01116 Contributes to Cisplatin Resistance in Lung Adenocarcinoma</p>

Six-long Non-coding RNA Signature to Predict the Prognosis of Lung Adenocarcinoma

Hypoxia‐induced factor‐1α promotes radioresistance of esophageal cancer cells by transcriptionally activating LINC01116 and suppressing miR‐3612 under hypoxia

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