[Retracted] miR‐30a‐5p Inhibits Proliferation and Migration of Lung Squamous Cell Carcinoma Cells by Targeting FOXD1

Chen, Chunhua; Tang, J; Xu, Shan; Zhang, Wenxia; Jiang, Hanliang

doi:10.1155/2020/2547902

Cited by 18 publications

(15 citation statements)

References 25 publications

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“…On this basis, this study revealed that miR-30a-5p may modulate ANLN in LUAD. Inactivated miR-30a-5p was discovered in different types of cancer including breast cancer [31], lung squamous cell car-cinoma [32], oral carcinoma [33], and clear cell renal cell carcinoma [34] and could work as a cancer suppressor. The present investigation illustrated evidently restrained miR-30a-5p in LUAD and its targeting ANLN.…”

Section: Discussionmentioning

confidence: 99%

ANLN Regulated by miR-30a-5p Mediates Malignant Progression of Lung Adenocarcinoma

Deng

Zhou

et al. 2021

Computational and Mathematical Methods in Medicine

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Background. ANLN and miR-30a-5p may be involved in the progression of lung adenocarcinoma (LUAD). However, their underlying mechanism in LUAD has not been completely comprehended. Methods. Differential expression analysis, binding site prediction, and survival analysis were conducted by bioinformatics approaches. ANLN mRNA and miR-30a-5p expression were detected by qRT-PCR. ANLN protein expression was detected by western blot. Cell behaviors in LUAD were examined by functional experiments. Results. ANLN was activated in LUAD cells in terms of mRNA and protein. High ANLN level was positively correlated with poor prognosis. Enforced ANLN stimulated protumorigenesis LUAD cell behaviors. miR-30a-5p could target ANLN mRNA, as revealed and verified through assays. Remarkably low miR-30a-5p expression was observed in LUAD cells, and it could repress ANLN expression. The accelerated cell behaviors by overexpression of ANLN were counteracted by upregulating miR-30a-5p. Conclusion. Overall, miR-30a-5p remarkably restrained the malignant progression of LUAD cells by constraining ANLN expression. Thus, ANLN and miR-30a-5p could be novel therapeutic targets of LUAD.

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Section: Discussionmentioning

confidence: 99%

ANLN Regulated by miR-30a-5p Mediates Malignant Progression of Lung Adenocarcinoma

Deng

Zhou

et al. 2021

Computational and Mathematical Methods in Medicine

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“…Consistently, miR-139-5p was downregulated in LUAD and exerted the ability to inhibit proliferation, migration, and invasion of cancer cells by targeting MAD2L1 [ 37 ]. Moreover, several studies have found that miR-30a-5p inhibited the proliferation of multiple cancers, such as breast cancer, glioma, and lung squamous cell carcinoma [ 38 – 40 ]. It is reported that miR-490-3p overexpression significantly inhibited the proliferation, invasion, and migration of hepatocellular carcinoma cells by activating BCYRN1 [ 41 ].…”

Section: Discussionmentioning

confidence: 99%

Identification of Differentially Expressed and Prognostic lncRNAs for the Construction of ceRNA Networks in Lung Adenocarcinoma

Cui

Liu

et al. 2021

Journal of Oncology

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Background. Long noncoding RNAs (lncRNAs) could function as competitive endogenous RNAs (ceRNAs) to competitively adsorb microRNAs (miRNAs), thereby regulating the expression of their target protein-coding mRNAs. In this study, we aim to identify more effective diagnostic and prognostic markers for lung adenocarcinoma (LUAD). Methods. We obtained differentially expressed lncRNAs (DElncRNAs), miRNAs (DEmiRNAs), and mRNAs (DEmRNAs) for LUAD by using The Cancer Genomes Atlas (TCGA) portal. Weighted gene coexpression network analysis (WGCNA) was performed to unveil core gene modules associated with LUAD. The Cox proportional hazards model was performed to determine the prognostic significance of DElncRNAs. The diagnostic and prognostic significance of DElncRNAs was further verified based on the receiver operating characteristic curve (ROC). Cytoscape was used to construct the ceRNA networks comprising the lncRNAs-miRNAs-mRNAs axis based on the correlation obtained from the miRcode, miRDB, and TargetScan. Results. Compared with normal lung tissues, 2355 DElncRNAs, 820 DEmiRNAs, and 17289 DEmRNAs were identified in LUAD tissues. We generated 8 WGCNA core modules in the lncRNAs coexpression network, 5 modules in the miRNAs, and 12 modules in the mRNAs coexpression network, respectively. One lncRNA module (blue) consisting of 441 lncRNAs, two miRNA modules (blue and turquoise) containing 563 miRNAs, and one mRNA module (turquoise), which consisted of 15162 mRNAs, were mostly significantly related to LUAD status. Furthermore, 67 DEmRNAs were found to be tumor-associated as well as the target genes of the DElncRNAs-DEmiRNAs axis. Survival analyses showed that 6 lncRNAs (LINC01447, WWC2-AS2, OGFRP1, LINC00942, LINC01168, and AC005863.1) were significantly correlated with the prognosis of LUAD patients. Ultimately, the potential ceRNA networks including 6 DElncRNAs, 4 DEmiRNAs, and 22 DEmRNAs were constructed. Conclusion. Our study indicated that 6 DElncRNAs had the possibilities as diagnostic and prognostic biomarkers for LUAD. The lncRNA-mediated ceRNA networks might provide novel insights into the molecular mechanisms of LUAD progression.

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“…Recent reports indicated that FOXD1 plays a oncogenic effect in several types of cancer [ 30 , 31 , 32 , 33 , 34 , 35 , 36 ] and likely associates with the mechanism for radioresistance [ 37 ]. In this study, our data showed that FOXD1 is capable of directly regulating the expression of G3BP2 , which is capable of inhibiting p53 activity through a direct binding, which may further promote p53 nuclear export via increasing p53 sumoylation [ 38 ] and serves as a poor prognostic marker in prostate cancer patients [ 39 ].…”

Section: Discussionmentioning

confidence: 99%

FOXD1 Repression Potentiates Radiation Effectiveness by Downregulating G3BP2 Expression and Promoting the Activation of TXNIP-Related Pathways in Oral Cancer

Lin

Lee

Chang

et al. 2020

Cancers

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Radiotherapy is commonly used to treat oral cancer patients in the current clinics; however, a subpopulation of patients shows poor radiosensitivity. Therefore, the aim of this study is to identify a biomarker or druggable target to enhance the effectiveness of radiotherapy on oral cancer patients. By performing an in silico analysis against public databases, we found that the upregulation of FOXD1, a gene encoding forkhead box d1 (Foxd1), is extensively detected in primary tumors compared to normal tissues and associated with a poor outcome in oral cancer patients receiving irradiation treatment. Moreover, our data showed that the level of FOXD1 transcript is causally relevant to the effective dosage of irradiation in a panel of oral cancer cell lines. The FOXD1 knockdown (FOXD1-KD) dramatically suppressed the colony-forming ability of oral cancer cells after irradiation treatment. Differentially expressed genes analysis showed that G3BP2, a negative regulator of p53, is predominantly repressed after FOXD1-KD and transcriptionally regulated by Foxd1, as judged by a luciferase-based promoter assay in oral cancer cells. Gene set enrichment analysis significantly predicted the inhibition of E2F-related signaling pathway but the activation of the interferons (IFNs) and p53-associated cellular functions, which were further validated by luciferase reporter assays in the FOXD1-KD oral cancer cells. Robustly, our data showed that FOXD1-KD fosters the expression of TXNIP, a downstream effector of IFN signaling and activator of p53, in oral cancer cells. These findings suggest that FOXD1 targeting might potentiate the anti-cancer effectiveness of radiotherapy and promote immune surveillance on oral cancer.

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[Retracted] miR‐30a‐5p Inhibits Proliferation and Migration of Lung Squamous Cell Carcinoma Cells by Targeting FOXD1

Cited by 18 publications

References 25 publications

ANLN Regulated by miR-30a-5p Mediates Malignant Progression of Lung Adenocarcinoma

ANLN Regulated by miR-30a-5p Mediates Malignant Progression of Lung Adenocarcinoma

Identification of Differentially Expressed and Prognostic lncRNAs for the Construction of ceRNA Networks in Lung Adenocarcinoma

FOXD1 Repression Potentiates Radiation Effectiveness by Downregulating G3BP2 Expression and Promoting the Activation of TXNIP-Related Pathways in Oral Cancer

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