The Essential Role of H19 Contributing to Cisplatin Resistance by Regulating Glutathione Metabolism in High-Grade Serous Ovarian Cancer

Zheng, Zhong; Xu, Hong; Suo, Shasha; Xu, Xin; Ni, Maowei; Gu, Linhui; Chen, Wei; Wang, Liangyan; Zhao, Ye; Teng, Bing; Hua, Yuejin

doi:10.1038/srep26093

Cited by 120 publications

(99 citation statements)

References 51 publications

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“…LUCAT1 has also been reported as a liver metastasis‐associated lncRNA through an analysis of CRC tissues from TCGA and Gene Expression Omnibus (GEO) databases; however, the underlying mechanisms are still unclear. Consistent with other studies, in which some lncRNAs including LUCAT1 are associated with chemotherapy resistance, our results revealed that LUCAT1 knockdown enhanced the apoptosis of CRC cells treated with oxaliplatin and 5‐FU.…”

Section: Discussionsupporting

confidence: 92%

“…Lung cancer‐associated transcript 1 is located on chromosome 5 and was first observed in the airway epithelium of smokers and in various cancer cell lines . In addition to lung cancer, LUCAT1 has also been reported to be involved in esophageal cancer, renal cell carcinoma, and cisplatin‐resistant ovarian cancer . Like other lncRNAs, LUCAT1 participates in carcinogenesis and cancer progression by regulating gene expression through chromatin modification, transcription, and post‐transcriptional procession.…”

Section: Discussionmentioning

confidence: 99%

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LUCAT1 promotes colorectal cancer tumorigenesis by targeting the ribosomal protein L40‐MDM2‐p53 pathway through binding with UBA52

et al. 2019

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Colorectal cancer ( CRC ) is the third most commonly diagnosed cancer in both men and women in the USA. However, the underlying molecular mechanisms that drive CRC tumorigenesis are still not clear. Several studies have reported that long noncoding RNA s (lnc RNA s) have important roles in tumor development. Here, we undertook a transcriptome microarray analysis in 6 pairs of CRC tissues and their corresponding adjacent normal tissues. A total of 1705 differentially expressed lnc RNA s were detected in CRC tissues at stages I/ II and III / IV (fold change greater than or equal to 2 or less than or equal to 0.5). Among them, we found that the lnc RNA lung cancer‐associated transcript 1 ( LUCAT 1 ) was upregulated in CRC tissues and was closely associated with poor overall survival of CRC patients, through analysis of clinical data and The Cancer Genome Atlas. Functional studies indicated that LUCAT 1 promoted CRC cell proliferation, apoptosis, migration, and invasion in vitro and in vivo. Furthermore, knockdown of LUCAT 1 rendered CRC cells hypersensitive to oxaliplatin treatment. Mechanistically, bioinformatic analysis indicated that low expression of LUCAT 1 was associated with the p53 signaling pathway. Chromatin isolation by RNA purification followed by mass spectrometry and RNA immunoprecipitation revealed that LUCAT 1 bound with UBA 52 , which encodes ubiquitin and 60S ribosomal protein L40 ( RPL 40). We found that RPL 40 functions in the ribosomal protein‐ MDM 2‐p53 pathway to regulate p53 expression. Taken together, our findings indicate that suppression of LUCAT 1 induces CRC cell cycle arrest and apoptosis by binding UBA 52 and activating the RPL 40‐ MDM 2‐p53 pathway. These results implicate LUCAT 1 as a potential prognostic biomarker and therapeutic target for CRC .

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Section: Discussionsupporting

confidence: 92%

Section: Discussionmentioning

confidence: 99%

LUCAT1 promotes colorectal cancer tumorigenesis by targeting the ribosomal protein L40‐MDM2‐p53 pathway through binding with UBA52

et al. 2019

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“…Clinical samples analysis showed that higher expression of LUCAT1 was associated with tumor size, tumornode-metastasis (TNM) stage and overall survival (OS). Besides, LUCAT1 also showed to modulate drug resistance [23,24]. To explore the potential molecular mechanisms of these lncRNA, we used GO and pathway analyses.…”

Section: Discussionmentioning

confidence: 99%

Long Non-Coding RNA Expression Profiles for the Characterization of Different Bladder Cancer Grade

Cao

Zhou

et al. 2018

Cell Physiol Biochem

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Background/Aims: Bladder cancer (BC) is one of the most frequent urologic tumors worldwide. However, long non-coding RNA(lncRNA) expression profiles in BC progression remain unclear. This study aimed to explore lncRNA expression profiles in different grades of bladder cancer and normal urothelium tissues. Methods: We performed high-throughput sequencing in BC tissues of different grade and obtained the expression profiles of its lncRNAs. Then, aberrantly expressed lncRNAs were validated by quantitative reverse transcription polymerase chain reaction (RT-PCR). Gene Ontology (GO) and pathway analyses were used to investigate the potential function of these lncRNAs. Co-expresson network was constructed to explore the relationship between lncRNAs and target mRNAs. Results: We identified 252 aberrantly expressed lncRNAs in high-grade BC while compared to low-grade BC, and 269 lncRNAs in high-grade BC while compared to normal urothelium. Notably, we found 33 overlapped lncRNAs. Subsequently, 7 lncRNAs were selected from the overlapped part and confirmed by RT-PCR. GO and pathway analyses showed that these dysregulated lncRNAs participated in cell migration, cell adhesion, as well as Ras signaling pathway. Co-expression network and The Cancer Genome Atlas (TCGA) data showed LUCAT1 and CCNB1 had positive relationship in regulating the progress of bladder cancer. Conclusion: Our findings revealed the significant role of lncRNAs in the development process of bladder cancer.

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“…[31][32][33][34] Our previous study revealed that H19 expression level, associated with its promoter methylation status, was significantly upregulated in CML patients involving in disease progression. 11,21 Therefore, it is important to illuminate the resistance mechanism and to overcome H19 is a long chain non-coding RNA with length of 2.3 kb.…”

Section: Discussionmentioning

confidence: 99%

“…Several studies have reported that overexpression of H19 was correlated with drug resistance in many tumors such as lung adenocarcinoma, ovarian cancer, human glioma, liver cancer. [31][32][33][34] Our previous study revealed that H19 expression level, associated with its promoter methylation status, was significantly upregulated in CML patients involving in disease progression. 35 Also, H19 was identified to be upregulated by DDX43 through demethylation related to CML progression.…”

Section: Discussionmentioning

confidence: 99%

Establishment and molecular characterization of decitabine‐resistant K562 cells

Wen

Zhang

et al. 2019

J Cellular Molecular Medi

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The clinical activity of decitabine (5‐aza‐2‐deoxycytidine, DAC), a hypomethylating agent, has been demonstrated in acute myeloid leukemia (AML) and myelodysplastic syndrome (MDS) patients. However, secondary resistance to this agent often occurs during treatment and leads to treatment failure. It is important to clarify the mechanisms underlying the resistance for improving the efficacy. In this study, by gradually increasing concentration after a continuous induction of DAC, we established the DAC‐resistant K562 cell line (K562/DAC) from its parental cell line K562. The proliferation and survival rate of K562/DAC was significantly increased, whereas the apoptosis rate was remarkably decreased than that of K562 after DAC treatment. In K562/DAC, a total of 108 genes were upregulated and 118 genes were downregulated by RNA‐Seq. In addition, we also observed aberrant expression of DDX43/H19/miR‐186 axis (increased DDX43 / H19 and decreased miR‐186 ) in K562/DAC cells. Ectopic expression of DDX43 in parental K562 cells rendered cells resistant to the DAC. Taken together, we successfully established DAC‐resistant K562 cell line which can serve as a good model for investigating DAC resistance mechanisms, and DDX43/H19/miR‐186 may be involved in DAC resistance in K562.

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The Essential Role of H19 Contributing to Cisplatin Resistance by Regulating Glutathione Metabolism in High-Grade Serous Ovarian Cancer

Cited by 120 publications

References 51 publications

LUCAT1 promotes colorectal cancer tumorigenesis by targeting the ribosomal protein L40‐MDM2‐p53 pathway through binding with UBA52

LUCAT1 promotes colorectal cancer tumorigenesis by targeting the ribosomal protein L40‐MDM2‐p53 pathway through binding with UBA52

Long Non-Coding RNA Expression Profiles for the Characterization of Different Bladder Cancer Grade

Establishment and molecular characterization of decitabine‐resistant K562 cells

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