Long Non-coding RNA PANDAR Promotes Radioresistance in Nasopharyngeal Carcinoma via SIRT1/Ku70/PI3K/Akt Pathway

2021 ◽  
Author(s):  
Si-wei Li ◽  
Guo-liang Pi ◽  
Yong Zeng ◽  
Chang-li Ruan ◽  
Xiao-song He ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Dna Damage ◽  
Nasopharyngeal Carcinoma ◽  
Sirtuin 1 ◽  
Akt Pathway ◽  
Phosphatidylinositol 3 Kinase ◽  
Normal Tissues ◽  
Non Coding Rna ◽  
Cancer Tissues ◽  
Long Non Coding Rna

Abstract Objective: Radioresistance may result in nasopharyngeal carcinoma (NPC) radiation failure. To comprehend the concrete mechanism in NPC radioresistance, this work was initiated from long non-coding RNA (lncRNA) promoter of CDKN1A antisense DNA damage activated RNA (PANDAR), accompanied by sirtuin 1 (SIRT1), Ku70, and phosphatidylinositol 3 kinase (PI3K)/Akt pathway.Methods: NPC cancer tissues and normal tissues were harvested and NPC cancer tissues were specified into radioresistant and radiosensitive types. The connection between PANDA expression with NPC radioresistance, clinicopathological traits and prognosis was tested. Radioresistant CNE2-IR and 5-8F-IR cells were induced and transfected with depleted PANDAR or SIRT1 to identify their roles in cell proliferation, cycle distribution, apoptosis, SIRT1, Ku70 and PI3K/Akt pathway. PANDA and SIRT1 expression in CNE2-IR and 5-8F-IR cells were tested.Results: PANDA was elevated in NPC tissues and radioresistant tissues relative to normal tissues and radiosensitive tissues. Raised PANDA was connected with NPC radioresistance and unsatisfactory prognosis. CNE2-IR and 5-8F-IR cells expressed up-regulated PANDA and SIRT1. Down-regulating PANDA or SIRT1 inhibited radioresistant NPC cell proliferation, decreased SIRT1 and Ku70, and inactivated PI3K/Akt pathway.Conclusion: This work has clued that depleting PANDA decreases SIRT1 recruitment to inactivate Ku70 deacetylation-mediated PI3K/Akt pathway, thereby promoting NPC radiosensitivity.

scholarly journals Long non-coding RNA LINC00152 regulates cell proliferation and migration by epigenetically repressing LRIG1 expression in cholangiocarcinoma

2020 ◽  
Author(s):  
Ni Wang ◽  
Yang Yu ◽  
Boming Xu ◽  
Chunmei Zhang ◽  
Jie Liu ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Biological Function ◽  
Rna Seq ◽  
Normal Tissues ◽  
Qrt Pcr ◽  
Non Coding Rna ◽  
And Migration ◽  
Long Non Coding Rna ◽  
Proliferation And Migration

Abstract Background: Recently, long non-coding RNAs (lncRNAs) have been verified to have significant regulatory roles in multiple human cancer processes. Long non-coding RNA LINC00152, located on chromosome 2p11.2, was identified as an oncogenic lncRNA in various cancers. However, the biological function and molecular mechanism of LINC00152 in cholangiocarcinoma (CCA) are still unknown.Methods: Bioinformatic analysis was performed to determine LINC00152 expression levels in the CCA and normal tissues by using raw microarray data downloaded from Gene Expression Omnibus (GSE76297) and The Cancer Genome Atlas (TCGA). Quantitative reverse transcription PCR (qRT-PCR) was used to validate LINC00152 expression in the CCA tissues compared with that in the paired normal tissues. CCK8, colony formation, Edu assays, transwell assays, flow cytometry, and in vivo tumor formation assays were performed to investigate the biological function of LINC00152 on CCA cell phenotypes. RNA-seq was carried out to identify the downstream target gene which was further examined by qRT-PCR, western bolt and rescue experiments. RNA immunoprecipitation (RIP) and Chromatin immunoprecipitation (ChIP) assays were performed to reveal the factors involved in the mechanism of LINC00152 functions in CCA.Results: LINC00152 is significantly upregulated in cholangiocarcinoma. LINC00152 regulated the proliferation and migration of cholangiocarcinoma cells both in vitro and in vivo. RNA-seq revealed that LINC00152 knockdown preferentially affected genes linked with cell proliferation, cell differentiation and cell adhesion. Furthermore, mechanistic investigation validated that LINC00152 could bind EZH2 and modulate the histone methylation of promoter of leucine rich repeats and immunoglobulin like domains 1 (LRIG1), thereby affecting cholangiocarcinoma cells growth and migration.Conclusion: Taken together, these results demonstrated the significant roles of LINC00152 in cholangiocarcinoma and suggested a new diagnostic and therapeutic direction of cholangiocarcinoma.

scholarly journals The pseudogene-derived long non-coding RNA SFTA1P suppresses cell proliferation, migration, and invasion in gastric cancer

2018 ◽  
Vol 38 (2) ◽  
Author(s):  
Hongwei Ma ◽  
Tianshi Ma ◽  
Miao Chen ◽  
Zigui Zou ◽  
Zhihong Zhang
Keyword(s):  
Gastric Cancer ◽  
Cell Proliferation ◽  
Human Cancer ◽  
Current Evidence ◽  
Migration And Invasion ◽  
Strongly Correlated ◽  
Normal Tissues ◽  
Advanced Tumor ◽  
Non Coding Rna ◽  
Long Non Coding Rna

Pseudogenes were once regarded as transcriptionally inactive and without specific molecular function. However, current evidence shows that pseudogene-derived long non-coding RNAs (lncRNAs) may be crucial regulators of human cancer development, including gastric cancer (GC). In the present study, we report that a pseudogene-derived lncRNA named surfactant associated 1, pseudogene (SFTA1P), which is 693-nt long, was significantly down-regulated in GC tissues compared with that in the adjacent normal tissues. In addition, decreased SFTA1P expression was strongly correlated with advanced tumor lymph node metastasis (TNM) stage, larger tumor size, lymphatic metastasis, and poor prognosis of patients with GC. Moreover, gain-of-function experiments revealed that the overexpression of SFTA1P inhibits cell proliferation, migration, and invasion, thus verifying the tumor inhibitory role of SFTA1P in GC. Furthermore, we investigated the potential action mechanism of SFTA1P. Our results showed that down-regulation of SFTA1P may be associated with decreased TP53 expression. In summary, our work suggests that the pseudogene-derived lncRNA SFTA1P functions as a tumor suppressor in GC and thus may act as a potential diagnostic and therapeutic target of GC.

scholarly journals ZFAS1 functions as an oncogenic long non-coding RNA in bladder cancer

2018 ◽  
Vol 38 (3) ◽  
Author(s):  
Haifan Yang ◽  
Ge Li ◽  
Bo Cheng ◽  
Rui Jiang
Keyword(s):  
Cell Proliferation ◽  
Bladder Cancer ◽  
Cancer Cell ◽  
Biological Function ◽  
Bladder Cancer Cell ◽  
Migration And Invasion ◽  
Cancer Cell Proliferation ◽  
Non Coding Rna ◽  
Cancer Tissues ◽  
Long Non Coding Rna

Long non-coding RNA (lncRNA) ZFAS1 (zinc finger antisense 1) has been suggested to have an oncogenic role in the tumorigenesis of human malignant tumors. However, the expression status and biological function of ZFAS1 in bladder cancer is still unknown. Thus, the purpose of the present study is to explore the clinical value of ZFAS1 in bladder cancer patients, and the biological function of ZFAS1 in bladder cancer cell. In the present study, we found ZFAS1 expression was increased in bladder cancer tissues compared with paired adjacent normal tissues through analyzing the Cancer Genome Atlas (TCGA) database. Furthermore, we confirmed that levels of ZFAS1 expression were elevated in bladder cancer tissues and cell lines compared with normal bladder tissues and normal uroepithelium cell line, respectively. Then, we observed that the expression level of ZFAS1 was positively associated with clinical stag, muscularis invasion, lymph node metastasis, and distant metastasis in bladder cancer patients. The experiments in vitro suggested that knockdown of ZFAS1 repressed bladder cancer cell proliferation via up-regulating KLF2 and NKD2 expression, and inhibited cell migration and invasion via down-regulating ZEB1 and ZEB2 expression. In conclusion, ZFAS1 is overexpressed in bladder cancer, and functions as an oncogenic lncRNA in regulating bladder cancer cell proliferation, migration, and invasion.

scholarly journals Long non-coding RNA MALAT1 promotes cholangiocarcinoma cell proliferation and invasion by activating PI3K/Akt pathway

Neoplasma ◽  
2017 ◽  
Vol 64 (05) ◽  
pp. 725-731 ◽  
Author(s):  
C. Wang ◽  
Z. p. Mao ◽  
L. Wang ◽  
G. h. Wu ◽  
F. h. Zhang ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Akt Pathway ◽  
Non Coding Rna ◽  
Cholangiocarcinoma Cell ◽  
Long Non Coding Rna ◽  
Proliferation And Invasion

scholarly journals The long non-coding RNA SNHG12 promotes gastric cancer by activating the phosphatidylinositol 3-kinase/AKT pathway

Aging ◽  
2019 ◽  
Vol 11 (23) ◽  
pp. 10902-10922 ◽  
Author(s):  
Rui Zhang ◽  
Yuan Liu ◽  
Hui Liu ◽  
Wei Chen ◽  
Hui-Ning Fan ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Akt Pathway ◽  
Phosphatidylinositol 3 Kinase ◽  
Non Coding Rna ◽  
Long Non Coding Rna ◽  
Phosphatidylinositol 3

Long non-coding RNA MIAT promotes cervical cancer proliferation and migration

2020 ◽  
Vol 168 (2) ◽  
pp. 183-190 ◽  
Author(s):  
Lei Zhang ◽  
Shuxia Ge ◽  
Bing Cao
Keyword(s):  
Cervical Cancer ◽  
Cell Proliferation ◽  
Cell Lines ◽  
Cell Model ◽  
Signalling Pathway ◽  
Migration And Invasion ◽  
Non Coding Rna ◽  
Cancer Tissues ◽  
Long Non Coding Rna ◽  
Proliferation And Invasion

Abstract Cervical cancer is one of the most common cancers in the world while its pathological mechanisms are not well-elucidated. Long non-coding RNA (lncRNA) has been implicated in cancer development. The dysregulation of lncRNA myocardial infarction-associated transcript (MIAT) has been reported in several cancers while its role in cervical cancer is not described yet. In this study, the role of MIAT in cervical cancer was explored. We evaluated the expression of MIAT in cervical cancer tissues and cell lines. Furthermore, we explored the effects of MIAT on proliferation and invasion of cervical cancer using cell model and animal transplantation model. We also evaluated the effects of MIAT on activation of PI3K/Akt/mTOR signalling pathway. Our results show that MIAT was up-regulated in cervical cancer tissues and cell lines. Knocking down MIAT resulted in decreased cell proliferation, migration and invasion of cervical cancer cells and suppression of tumour growth in mice. Mechanically, knocking down MIAT suppressed the activation of PI3K/Akt signalling pathway. In conclusion, MIAT promotes cell proliferation and invasion in cervical cancer.

LINK-A long non-coding RNA and VEGF RNA expression in epithelial ovarian cancer patients

2020 ◽  
Vol 28 (3) ◽  
pp. 227-232
Author(s):  
Parichehr Maleki ◽  
Sadaf Valeh Sheida ◽  
Seyed Javad Mowla ◽  
Vahid Soleimani ◽  
Mohammad Taheri ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Epithelial Ovarian Cancer ◽  
P Value ◽  
Rna Expression ◽  
Vegf Mrna ◽  
Kinase Activation ◽  
Normal Tissues ◽  
Non Coding Rna ◽  
Cancer Tissues ◽  
Long Non Coding Rna

LINK-A (long intergenic non-coding RNA for kinase activation) is a newly identified long non-coding RNA with oncogenic function, which leads to the hyperactivation of AKT and HIF1α. thereby, fosters cell proliferation, mobility and metastasis. VEGF (vascular endothelial growth factor), a well-known cytokine has an important role in angiogenesis. In this study, we quantified RNA expression of LINK-A and VEGF on 45 tumor specimens obtained from Iranian patients diagnosed with Epithelial Ovarian Cancer (EOC). Our goal was to evaluate expression of LINK-A lncRNA and VEGF mRNA in ovarian cancer tissues and find the probable correlation of LINK-A with VEGF as a major transcription target for HIF1α. LINK-A and VEGF were remarkably overexpressed in EOC tissues compared to normal tissues (P value: 0.004, 0.0001, respectively), but we did not find correlation between LINK-A and VEGF RNA expressions in this study. LINK-A was significantly overexpressed in higher stages of cancer and tumor grades. VEGF was only significantly elevated in higher stages. This study confirms importance of novel lncRNA of LINK-A in Iranian EOC patients.

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