&lt;p&gt;LncRNA PVT1 Enhances Proliferation and Cisplatin Resistance via Regulating miR-194-5p/HIF1a Axis in Oral Squamous Cell Carcinoma&lt;/p&gt;

Wang, Fang; X, Ji; Wang, Jingjing; Ma, Xiangrui; Yong, Yang; Zuo, Jinhua; Cui, Jun

doi:10.2147/ott.s232405

Cited by 37 publications

(18 citation statements)

References 32 publications

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“…Its aberrant expression can be a relatively independent regulatory factor for promoting tumorigenesis and MYC [ 22 , 23 , 24 ]. The upregulation of PVT1 suggests that it can be used for the early detection of cancer, the prognostication of drug resistance, or as a therapeutic target [ 25 , 26 ].…”

Section: Introductionmentioning

confidence: 99%

LncRNA PVT1 Is a Poor Prognosticator and Can Be Targeted by PVT1 Antisense Oligos in Gastric Adenocarcinoma

Song

Pizzi

et al. 2020

Cancers

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Gastric adenocarcinoma (GAC) is inherently resistant or becomes resistant to therapy, leading to a poor prognosis. Mounting evidence suggests that lncRNAs can be used as predictive markers and therapeutic targets in the right context. In this study, we determined the role of lncRNA-PVT1 in GAC along with the value of inhibition of PVT1 using antisense oligos (ASOs). RNA scope in situ hybridization was used to analyze PVT1 expression in tumor tissue microarrays (TMAs) of GAC and paired normal tissues from 792 patients. Functional experiments, including colony formation and invasion assays, were performed to evaluate the effects of PVT1 ASO inhibition of PVT1 in vitro; patient-derived xenograft models were used to evaluate the anti-tumor effects of PVT1 ASOs in vivo. LncRNA-PVT1 was upregulated in GACs compared to the matched adjacent normal tissues in the TMA. LncRNA PVT1 expression was positively correlated with larger tumor size, deeper wall invasion, lymph node metastases, and short survival duration. Inhibition of PVT1 using PVT1 ASOs significantly suppressed tumor cell growth and invasion in vitro and in vivo. PVT1 expression was highly associated with poor prognosis in GAC patients and targeting PVT1 using PVT1 ASOs was effective at curtailing tumor cell growth in vitro and in vivo. Thus, PVT1 is a poor prognosticator as well as therapeutic target. Targeting PVT1 using PVT1 ASOs provides a novel therapeutic strategy for GAC.

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Section: Introductionmentioning

confidence: 99%

LncRNA PVT1 Is a Poor Prognosticator and Can Be Targeted by PVT1 Antisense Oligos in Gastric Adenocarcinoma

Song

Pizzi

et al. 2020

Cancers

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“… 10 Previous research demonstrated that lncRNA plays a pivotal role in diverse biological processes, including tumorigenesis and cancer progression. 7 , 21 , 22 Aberrantly expressed lncRNAs are observed in OSCC. For instance, lncRNA AC007271.3, highly expressed in OSCC, expedites cancer cell proliferation, migration and invasion, and represses apoptosis via regulating Wnt/β-catenin signaling; 23 lncRNA CASC9, associated with tumor size and metastasis, works as a potential biomarker of detrimental prognosis of OSCC patients.…”

Section: Discussionmentioning

confidence: 99%

LINC00662 Promotes Oral Squamous Cell Carcinoma Cell Growth and Metastasis through miR-144-3p/EZH2 Axis

Yao¹,

Liu²,

Jin

et al. 2021

Yonsei Med J

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Purpose Long non-coding RNA (lncRNA) is identified as an important regulator involved in oral squamous cell carcinoma (OSCC) tumorigenesis. This study aimed to investigate the functional role and underlying mechanism of LINC00662 in OSCC. Materials and Methods The expression levels of LINC00662, miR-144-3p, and enhancer of zeste homolog 2 (EZH2) mRNA were quantified with quantitative real-time polymerase chain reaction in OSCC tissues and cell lines. Western blot analysis was used to assay the expression levels of E-cadherin, Vimentin, and EZH2. Cell proliferation, migration, and invasion were monitored by cell counting kit-8 and Transwell assays. Dual-luciferase reporter and RNA immunoprecipitation assays were employed to verify the regulatory relationship between LINC00662 and miR-144-3p. Results The expression of LINC00662, positively associated with the increased TNM stage and lymph node metastasis of the patients, was up-regulated in OSCC tissues and cells. The overexpression of LINC00662 facilitated the proliferation, migration, and invasion of OSCC cells. MiR-144-3p could bind to LINC00662, and the promoting effect of LINC00662 overexpression was counteracted by miR-144-3p mimic. Moreover, EZH2 expression was negatively regulated by miR-144-3p and positively regulated by LINC00662. The silencing of EZH2 attenuated the promoting effects of overexpression of LINC00662 on cell proliferation, migration, invasion, and epithelial-mesenchymal transition. Conclusion LINC00662, as an oncogenic lncRNA of OSCC, accelerates OSCC progression by repressing miR-144-3p expression and increasing EZH2 expression.

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“…lncRNA plays a significant role in OSCC chemoresistance. 25 , 26 Therefore, we ran IC 50 assays to examine the sensitivity of oncolytic adenoviruses and chemotherapy drugs to OSCC so as to determine the role of SNHG1 in tumor treatment. We found that oncolytic adenovirus H101 exhibited higher sensitivity in OSCC with high SNHG1 expression and chemotherapy exhibited higher sensitivity in OSCC with low SNHG1 expression.…”

Section: Discussionmentioning

confidence: 99%

Overexpression of LncRNA SNHG1 Were Suitable for Oncolytic Adenoviruse H101 Therapy in Oral Squamous-Cell Carcinoma

Wang¹,

Song²,

Lv³

et al. 2020

OTT

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Background As the most prevalent type of head and neck cancer, oral squamous-cell carcinoma (OSCC) accounts for nearly 90% of all oral cancer cases. Despite great progress having been made in the diagnosis and treatment of OSCC recently, the survival rate of OSCC patients has not risen remarkably. Chemotherapy is commonly used for OSCC treatment; however, the emergence of chemoresistance limits its long-term curative effect. Therefore, identifying effective biomarkers and molecular mechanisms is essential to the development of therapeutic strategies for OSCC. Methods qRT-PCR assays were performed to detect SNHG1 expression in OSCC tissue and cells, and CCK8 assays and animal experiments used to examine cell proliferation. In addition, CCK8 assays were used to detect IC 50 values of cisplatin, 5Fu, Dox, and oncolytic adenovirus H101. Results We found that SNHG1 was overexpressed in OSCC tissue and cells and was associated with OSCC progression. In addition, knockdown of SNHG1 suppressed cell proliferation in vitro and in vivo. Importantly, we found that oncolytic adenovirus H101 showed better antitumor effects in OSCC with high SNHG1 expression, and chemotherapy showed worse anti-tumor effects in OSCC with high SNHG1 expression. Conclusion SNHG1 can act as a diagnostic biomarker for OSCC, and may be a biomarker for treatment options.

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<p>LncRNA PVT1 Enhances Proliferation and Cisplatin Resistance via Regulating miR-194-5p/HIF1a Axis in Oral Squamous Cell Carcinoma</p>

Cited by 37 publications

References 32 publications

LncRNA PVT1 Is a Poor Prognosticator and Can Be Targeted by PVT1 Antisense Oligos in Gastric Adenocarcinoma

LncRNA PVT1 Is a Poor Prognosticator and Can Be Targeted by PVT1 Antisense Oligos in Gastric Adenocarcinoma

LINC00662 Promotes Oral Squamous Cell Carcinoma Cell Growth and Metastasis through miR-144-3p/EZH2 Axis

Overexpression of LncRNA SNHG1 Were Suitable for Oncolytic Adenoviruse H101 Therapy in Oral Squamous-Cell Carcinoma

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