LncRNA ID2-AS1 suppresses tumor metastasis by activating the HDAC8/ID2 pathway in hepatocellular carcinoma

Zhou, Yuqiang; Huan, Lin; Wu, Yangjun; Bao, Chunyang; Chen, Bing; Wang, Lu; Huang, Shenglin; Liang, Linhui; He, Xianghuo

doi:10.1016/j.canlet.2019.11.007

Cited by 62 publications

(40 citation statements)

References 42 publications

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“…LncRNAs are > 200 nt long and do not encode proteins [ 15 ], yet can post-transcriptionally regulate diverse biological processes in many forms of cancer [ 16 – 18 ]. Increasing evidences have shown lncRNAs to control invasion, metastasis, differentiation, apoptosis, cell cycle progression, and tumor development [ 19 – 22 ]. An increasing number of lncRNAs, including lncRNA MEG3, lncRNA UCA1, and lncRNA LINC00511, are related to OC onset and progression [ 23 – 25 ].…”

Section: Introductionmentioning

confidence: 99%

LncRNA WDFY3-AS2 promotes cisplatin resistance and the cancer stem cell in ovarian cancer by regulating hsa-miR-139-5p/SDC4 axis

Wang

Xia

et al. 2021

Cancer Cell Int

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Background Ovarian cancer (OC) is a high-mortality gynecological cancer that is typically treated with cisplatin, although such treatment often results in chemoresistance. Ovarian cancer resistance is usually related to cell stemness. Herein, we explored the function of lncRNA WDFY3-AS2 in OC cell resistance to cisplatin (DDP). Methods Cisplatin resistant OC A2780 cell lines (A2780-DDP) were established by long-term exposure to cisplatin. CCK-8 assay were performed to evaluate the viability of A2780, and A2780-DDP cells. Quantitative RT-PCR was used to examine the expression of lncRNA WDFY3-AS2, miR-139-5p, and SDC4 in A2780-DDP cell lines. After treatment with cisplatin, cell apoptosis and CD44+CD166+-positive cells were measured by flow cytometry. The transwell assays were employed to measure the effect of WDFY3-AS2 on cell migration, and invasion. In addition, tumorsphere formation assay was used to enrich OC cancer stem cells (CSCs) from A2780-DDP cells. The expression of CSC markers (SOX2, OCT4, and Nanog) was detected by western blotting. The regulatory mechanism was confirmed by RNA pull down, and luciferase reporter assays. Furthermore, xenograft tumor in nude mice was used to assess the impact of WDFY3-AS2 on cisplatin resistance in OC in vivo. Results WDFY3-AS2 was highly expressed in OC A2780-DDP cells, and silencing WDFY3-AS2 significantly inhibited proliferation, migration and invasion but increased apoptosis in OC A2780-DDP cells. Additionally, WDFY3-AS2 significantly promoted the A2780-DDP cells tumorspheres. WDFY3-AS2 was predicted to impact OC by sponging miR-139-5p and regulating SDC4. The xenografts inoculated with A2780-DDP cells additionally confirmed that tumor growth in vivo was reduced by si-WDFY3-AS2 transfection. MiR-139-5p inhibitor or SDC4 overexpression could restore the suppressive influence of silenced WDFY3-AS2 on tumor growth. Conclusions Together, WDFY3-AS2 may lead to change of cisplatin resistance by the expression of miR-139-5p/SDC4 in the OC A2870-DDP cells both in vitro and in vivo. Our finding may provide a drug target for the drug resistance of OC.

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Section: Introductionmentioning

confidence: 99%

LncRNA WDFY3-AS2 promotes cisplatin resistance and the cancer stem cell in ovarian cancer by regulating hsa-miR-139-5p/SDC4 axis

Wang

Xia

et al. 2021

Cancer Cell Int

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“…Long non-coding R NAs (lncR NAs) a re typically >200 nucleotide-long RNAs without protein-coding potential (4). Growing evidence suggest that lncRNAs serve an important role in the regulation of cell proliferation, survival, apoptosis, invasion and migration and therefore serve a key role in cancer development (5)(6)(7). An increasing number of lncRNAs, including lncRNA MAGI2-AS3, lncRNA UCA1 and lncRNA LINC01355, have been associated with the progression of breast cancer (8)(9)(10).…”

Section: Introductionmentioning

confidence: 99%

lncRNA FGD5‑AS1 promotes breast cancer progression by regulating the hsa‑miR‑195‑5p/NUAK2 axis

Fang

Jiang

et al. 2021

Mol Med Rep

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Breast cancer is the second most prevalent cancer in women worldwide. Long non-coding RNAs (lncRNAs) have been identified as important regulators of tumorigenesis and tumor metastasis. lncRNA FGD5-AS1 has been previously reported as a carcinogenic gene, however its role in breast cancer has yet to be investigated. The present study aimed to understand the function of lncRNA FGD5-AS1 in breast cancer and examine the underlying molecular mechanisms. Sample tissues for downstream gene expression profiling were collected from patients with breast cancer (n=23). The effect of FGD5-AS1 overexpression on cell viability, invasion and migration has been studied in breast cancer cells (MDA-MB-231). Changes in glycolysis were monitored by comparing glucose consumption, lactate production and ATP levels. Using StarBase and TargetScan databases a putative interaction between FGD5-AS1, miR-195-5p and SNF1-like kinase 2 (NUAK2) was predicted in silico . Expression levels of FGD5-AS1, has-miR-195-5p and NUAK2 were validated by reverse transcription-quantitative PCR and interactions were validated using dual-luciferase reporter assays and RNA pull-down. High expression of lncRNA FGD5-AS1 was detected in breast cancer tissue samples and disease model cell lines. Silencing of FGD5-AS1 led to decreased cell proliferation, migration and invasion. It was identified that at a molecular level FGD5-AS1 serves as a sponge of miR-195-5p and alters the expression of its downstream target gene NUAK2. In breast cancer lncRNA FGD5-AS1 serve a key role in glycolysis and tumor progression via the miR-195-5p/NUAK2 axis. The findings of the present study indicated FGD5-AS1 as a candidate target for intervention in patients with breast cancer.

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“…LINC02397 has been reported to be involved in metastatic melanoma [ 34 ]. AC009495.2 suppresses tumour metastasis by activating the HDAC8/ID2 pathway in hepatocellular carcinoma [ 40 ]. RP11–326C3.2 is involved in breast cancer (ER/PR positive type) by interaction with RAS associated genes [ 48 ] and plays role during human erythroid differentiation [ 49 ].…”

Section: Discussionmentioning

confidence: 99%

lncRNAs–mRNAs Co–Expression Network Underlying Childhood B–Cell Acute Lymphoblastic Leukaemia: A Pilot Study

Affinito

Pane

Smaldone

et al. 2020

Cancers

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Long non–coding RNAs (lncRNAs) are emerging as key gene regulators in the pathogenesis and development of various cancers including B lymphoblastic leukaemia (B–ALL). In this pilot study, we used RNA–Seq transcriptomic data for identifying novel lncRNA–mRNA cooperative pairs involved in childhood B–ALL pathogenesis. We conceived a bioinformatic pipeline based on unsupervised PCA feature extraction approach and stringent statistical criteria to extract potential childhood B–ALL lncRNA signatures. We then constructed a co–expression network of the aberrantly expressed lncRNAs (30) and protein–coding genes (754). We cross–validated our in–silico findings on an independent dataset and assessed the expression levels of the most differentially expressed lncRNAs and their co–expressed mRNAs through ex vivo experiments. Using the guilt–by–association approach, we predicted lncRNA functions based on their perfectly co–expressed mRNAs (Spearman’s correlation) that resulted closely disease–associated. We shed light on 24 key lncRNAs and their co–expressed mRNAs which may play an important role in B–ALL pathogenesis. Our results may be of clinical utility for diagnostic and/or prognostic purposes in paediatric B–ALL management.

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LncRNA ID2-AS1 suppresses tumor metastasis by activating the HDAC8/ID2 pathway in hepatocellular carcinoma

Cited by 62 publications

References 42 publications

LncRNA WDFY3-AS2 promotes cisplatin resistance and the cancer stem cell in ovarian cancer by regulating hsa-miR-139-5p/SDC4 axis

LncRNA WDFY3-AS2 promotes cisplatin resistance and the cancer stem cell in ovarian cancer by regulating hsa-miR-139-5p/SDC4 axis

lncRNA FGD5‑AS1 promotes breast cancer progression by regulating the hsa‑miR‑195‑5p/NUAK2 axis

lncRNAs–mRNAs Co–Expression Network Underlying Childhood B–Cell Acute Lymphoblastic Leukaemia: A Pilot Study

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