&lt;p&gt;Long Non-Coding RNA SPRY4-IT1 Reverses Cisplatin Resistance by Downregulating MPZL-1 via Suppressing EMT in NSCLC&lt;/p&gt;

Ye, Yunyao; Gu, Jianqin; Liu, Pei; Wang, He; Jiang, Lihua; Lei, Tianyao; Yu, Shanxun; Han, Gaohua; Wang, Zhaoxia

doi:10.2147/ott.s232769

Cited by 21 publications

(14 citation statements)

References 28 publications

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“…[11][12][13][14] Increasing evidence has demonstrated the involvement of LncRNA in cisplatin resistance in multiple human cancers. [47][48][49][50][51] In NSCLC, LncRNA SPRY4-IT1 was reported to reverse cisplatin resistance partially through downregulating MPZL-1 via EMT, 52 and LncRNA NORAD was found to increase cisplatin resistance via the miR-129-1-3p/SOX4 axis. 53 A recent study concluded that LncRNA-XIST contributes to cisplatin resistance through down-regulating miRNA-144-3p.…”

Section: Discussionmentioning

confidence: 99%

LncRNA LINC01116 Contributes to Cisplatin Resistance in Lung Adenocarcinoma

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%

LncRNA LINC01116 Contributes to Cisplatin Resistance in Lung Adenocarcinoma

Wang¹,

Gao²,

Chen³

et al. 2020

OTT

Self Cite

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“…A significant body of evidence has indicated that lncRNAs are aberrantly expressed in NSCLC, which results in cancer progression, unlimited growth, and metastasis. [39][40][41] Moreover, lncRNAs have been identified as contributors to NSCLC etiology and development. 42,43 Therefore, investigating the regulatory activities of lncRNAs in NSCLC may lead to the identification of diagnostic markers and therapeutic targets for this fatal disease.…”

Section: Discussionmentioning

confidence: 99%

Long Noncoding RNA LINC01426 Sequesters microRNA-519d-5p to Promote Non-Small Cell Lung Cancer Progression by Increasing ETS1 Expression

Dai

Wang

Zhao

et al. 2020

CMAR

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Purpose Recent studies have identified important roles for long intergenic non-protein coding RNA 1426 ( LINC01426 ) in glioma and clear cell renal cell carcinoma. The present study evaluated the expression profile of LINC01426 in non-small cell lung cancer (NSCLC) tissues and cell lines. Furthermore, the function of LINC01426 in NSCLC and the molecular mechanisms involved were extensively studied. Methods The abundance of LINC01426 in NSCLC tissues and cell lines was determined using quantitative reverse transcription–polymerase chain reaction. The cell counting kit-8 assay, flow cytometry, transwell experiments for migration and invasion, and xenograft tumor model were used to assess the function of LINC01426 in NSCLC cells. Mechanistic studies were performed using the luciferase reporter assay and RNA immunoprecipitation. Results Significant LINC01426 upregulation was observed in NSCLC tissues and cell lines. Silencing LINC01426 inhibited proliferation, migration, and invasion of NSCLC cells and facilitated cell apoptosis in vitro. Furthermore, interference of LINC01426 restricted tumor growth of NSCLC cells in vivo. In addition, LINC01426 showed the ability to directly bind to microRNA-519d-5p (miR-519d-5p) and act as a molecular sponge for miR-519d-5p in NSCLC cells. Furthermore, the ETS proto-oncogene 1 ( ETS1 ) was identified as a direct target of miR-519d-5p and LINC01426 could indirectly upregulate ETS1 expression by sponging miR-519d-5p. Moreover, the cancer-inhibiting activities of LINC01426 knockdown in NSCLC cells were partially offset by miR-519d-5p inhibition. Conclusion LINC01426 increases ETS1 expression by sequestering miR-519d-5p, thereby aggravating the malignant progression of NSCLC. The LINC01426/miR-519d-5p/ETS1 competing endogenous RNA pathway may provide a target for designing therapeutic agents for NSCLC treatment.

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“…In general, SPRY4-IT seems to act in a pro-tumorigenic sense, being associated to the development and progression of several tumors, among which breast cancer ( 121 , 122 ), osteosarcoma ( 123 , 124 ), and colorectal cancer ( 125 , 126 ). However, there are some cases in which SPRY4-IT4 has been reported to act as a tumor suppressor, in particular in non-small cell lung cancer ( 127 , 128 ).…”

Section: Long Non-coding Rnas Role In Testicular Cancermentioning

confidence: 99%

Long Non-Coding RNAs: Role in Testicular Cancers

et al. 2021

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In the last few years lncRNAs have gained increasing attention among the scientific community, thanks to the discovery of their implication in many physio-pathological processes. In particular, their contribution to tumor initiation, progression, and response to treatment has attracted the interest of experts in the oncologic field for their potential clinical application. Testicular cancer is one of the tumors in which lncRNAs role is emerging. Said malignancies already have very effective treatments, which although lead to the development of quite serious treatment-related conditions, such as secondary tumors, infertility, and cardiovascular diseases. It is therefore important to study the impact of lncRNAs in the tumorigenesis of testicular cancer in order to learn how to exploit them in a clinical setting and to substitute more toxic treatments. Eventually, the use of lncRNAs as biomarkers, drug targets, or therapeutics for testicular cancer may represent a valid alternative to that of conventional tools, leading to a better management of this malignancy and its related conditions, and possibly even to the treatment of poor prognosis cases.

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<p>Long Non-Coding RNA SPRY4-IT1 Reverses Cisplatin Resistance by Downregulating MPZL-1 via Suppressing EMT in NSCLC</p>

Cited by 21 publications

References 28 publications

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

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

<p>Long Noncoding RNA LINC01426 Sequesters microRNA-519d-5p to Promote Non-Small Cell Lung Cancer Progression by Increasing ETS1 Expression</p>

Long Non-Coding RNAs: Role in Testicular Cancers

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