Long noncoding RNA FOXD3‐AS1 promotes colon adenocarcinoma progression and functions as a competing endogenous RNA to regulate SIRT1 by sponging miR‐135a‐5p

Wu, Qiong; Shi, Min; Wu, Meng; Wang, Yugang; Hui, Pingping; Ma, Jun

doi:10.1002/jcp.28752

Cited by 50 publications

(41 citation statements)

References 39 publications

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“…For instance, Zhang et al demonstrated that miR‐135a could accelerate cell growth and proliferation of lung cancer, but repress cell apoptosis . In colon adenocarcinoma, miR‐135a was suggested to be a "sponge" of lncRNA FOXD3‐AS1 to regulate cell proliferation, migration, invasion, and apoptosis by targeting SIRT1 . In addition, several studies have also revealed that the positive effects of miR‐135a on BC cell proliferation, epithelial‐mesenchymal transition, migration and invasion .…”

Section: Discussionmentioning

confidence: 99%

LncRNA MBNL1‐AS1 represses cell proliferation and enhances cell apoptosis via targeting miR‐135a‐5p/PHLPP2/FOXO1 axis in bladder cancer

et al. 2019

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LncRNAs have been shown to play essential roles in bladder cancer (BC) progress.Our microarrays of clinical samples firstly screened that lncRNA muscleblind-like 1 antisense RNA 1 (MBNL1-AS1) was poorly expressed in BC tissues. However, its biological function in BC remains not well understood. Here we examined the clinical correlations with MBNL1-AS1 in BC patients. Then, 5673 and T24 cell lines were employed to investigate the role of MBNL1-AS1 in the proliferation and apoptosis of BC cells in vitro and in vivo. Furthermore, miR-135a-5p (miR-135a)/PHLPP2/FOXO1 axis was focused to explore its regulatory mechanism in BC.The results showed that MBNL1-AS1 was significantly downregulated in bladder tumor tissues, and associated with BC progression. In vitro, MBNL1-AS1 knockdown increased the number of viable cells and bromodeoxyuridine-positive cells, accelerated cell cycle, and dysregulated proliferative regulators (Ki67, p21, p27, and Cyclin D1) in BC cells. The apoptotic cells and the cleavages of caspase-3/9 were reduced in MBNL1-AS1-silenced BC cells. Overexpression of MBNL1-AS1 had opposite effects on BC cell proliferation and apoptosis. Moreover miR-135a was demonstrated to interact with MBNL1-AS1, and inhibiting miR-135a reversed the effects of shMBNL1-AS1 on BC cells. The downstream effectors (PHLPP2 and FOXO1) were positively regulated by MBNL1-AS1, but negatively regulated by miR-135a. Similar results were also observed in xenograft tumors. In conclusion, this study firstly suggests that MBNL1-AS1 acts as a tumor suppressor of BC by targeting miR-135a/PHLPP2/FOXO1 axis, providing a novel insight for BC diagnosis and treatment. K E Y W O R D S bladder cancer, FOXO1, MBNL1-AS1, miR-135a-5p, PHLPP2 | 725 WEI Et al.

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Section: Discussionmentioning

confidence: 99%

LncRNA MBNL1‐AS1 represses cell proliferation and enhances cell apoptosis via targeting miR‐135a‐5p/PHLPP2/FOXO1 axis in bladder cancer

et al. 2019

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“…FOXD3-AS1 was abundantly expressed in both colorectal cancer (CRC) tissues and cells, FOXD3-AS1 overexpression was associated with worse clinical outcomes of CRC patients. In addition, silence of FOXD3-AS1 was effective in suppressing CRC cell progression [ 15 ]. In this study, we first showed that FOXD3-AS1 was up-regulated in A549/DDP and H1229/DDP cells compared to their corresponding parental NSCLC cells.…”

Section: Discussionmentioning

confidence: 99%

“…LncRNA EGFR antisense RNA 1 (EGFR-AS1) was found to be elevated in plasma of NSCLC patients and EGFR-AS1 overexpression promoted cisplatin resistance in NSCLC [ 11 ]. Recent evidence implied that lncRNA FOXD3 antisense RNA1 (FOXD3-AS1) was involved in the progression of different malignancies [ 12 – 15 ]. Unfortunately, little is known about FOXD3-AS1 regarding chemo-resistance in NSCLC.…”

Section: Introductionmentioning

confidence: 99%

LncRNA FOXD3-AS1 promoted chemo-resistance of NSCLC cells via directly acting on miR-127-3p/MDM2 axis

et al. 2020

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Background: This study aims to investigate the mechanism underlying the high level of long non-coding RNA FOXD3-AS1 in cisplatin-resistant NSCLC cells. Methods: Cisplatin-resistant cells were generated from A549 cells. CCK-8 were used to evaluate cell proliferation. The FOXD3-AS1, miR-127-3p, MDM2 and MRP1 mRNA expression levels were confirmed by qRT-PCR. Protein levels of MDM2 and MRP1 were determined by western blot assay. Luciferase reporter and RNA pull-down assays were evaluated the relationship between miR-127-3p and FOXD3-AS1/MDM2. In vivo tumor growth was evaluated in a xenograft nude mice model. Results: FOXD3-AS1 was up-regulated in cisplatin-resistant NSCLC cells (A549/DDP and H1299/DDP cells) in comparison with their parental cell lines. Overexpression of FOXD3-AS1 promoted cisplatin-resistance in A549 and H1299 cells; while FOXD3-AS1 knockdown sensitized A549/DDP and H1299/DDP cells to cisplatin treatment. FOXD3-AS1 regulated miR-127-3p expression by acting as a competing endogenous RNA, and miR-127-3p repressed MDM2 expression via targeting the 3′UTR. MiR-127-3p overexpression and MDM2 knockdown both increased the chemo-sensitivity in A549/DDP cells; while miR-127-3p knockdown and MDM2 overexpression both promoted chemoresistance in A549 cells. Further rescue experiments revealed that miR-127-3p knockdown or MDM2 overexpression counteracted the suppressive effects of FOXD3-AS1 knockdown on chemo-resistance and MRP1 expression in A549/DDP cells. In vivo studies showed that FOXD3-AS1 knockdown potentiated the antitumor effects of cisplatin treatment. Inspection of clinical samples showed the upregulation of FOXD3-AS1 and MDM2, and down-regulation of miR-127-3p in NSCLC tissues compared to normal adjacent tissues. Conclusion: In conclusion, our results suggest that LncRNA FOXD3-AS1 promotes chemo-resistance of NSCLC cells via directly acting on miR-127-3p/MDM2 axis. Our findings may provide novel perspectives for the treatment of NSCLC in patients resistant to chemotherapy.

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“…miR-135a and miR-9 are known to target SIRT1 expression 37 . Several studies have indicated that SIRT1 protects against stress-related diseases by interacting with p53, forkhead box protein (FOXO), NFκB and peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α), which regulate diverse cellular processes, including stress responses and inflammation 56,57 . In addition, the expression level of miR-25 increased in serum and lesion samples from vitiligo patients 47 .…”

Section: Mirnas Associated With Oxidative Stress In Vitiligomentioning

confidence: 99%

The Role of MicroRNAs in Vitiligo: Regulators and Therapeutic Targets

2020

Ann Dermatol

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Vitiligo is an acquired skin disorder clinically characterized by the progressive appearance of white maculae due to a loss of functioning epidermal melanocytes. Studies have shown that microRNAs (miRNAs) modulate cellular differentiation, proliferation and apoptosis, including immune cell and melanocyte development and functions. The role of miRNAs in the pathogenesis of several immune-related diseases has been explored. Novel approaches to target miRNAs have recently emerged allowing modulation of miRNAs levels in diverse pathological processes, thus making them promising targets for molecular-based diagnostics and therapy. Here, we report the present status of research on miRNAs expression and functional alterations in vitiligo, in order to more fully understand the role of these molecules in vitiligo pathology.

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Long noncoding RNA FOXD3‐AS1 promotes colon adenocarcinoma progression and functions as a competing endogenous RNA to regulate SIRT1 by sponging miR‐135a‐5p

Cited by 50 publications

References 39 publications

LncRNA MBNL1‐AS1 represses cell proliferation and enhances cell apoptosis via targeting miR‐135a‐5p/PHLPP2/FOXO1 axis in bladder cancer

LncRNA MBNL1‐AS1 represses cell proliferation and enhances cell apoptosis via targeting miR‐135a‐5p/PHLPP2/FOXO1 axis in bladder cancer

LncRNA FOXD3-AS1 promoted chemo-resistance of NSCLC cells via directly acting on miR-127-3p/MDM2 axis

The Role of MicroRNAs in Vitiligo: Regulators and Therapeutic Targets

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