Knockdown of DDX5 Inhibits the Proliferation and Tumorigenesis in Esophageal Cancer

Ma, Zhenchuan; Feng, Jie; Guo, Yurui; Kong, Ranran; Ma, Yuefeng; Sun, Liangzhang; Yang, Xiaoping; Zhou, Bin; Li, Shaomin; Zhang, Wei; Jiang, Jiantao; Zhang, Jin; Qiao, Zhe; Cheng, Yong; Zha, Danjie; Liu, Shiyuan

doi:10.3727/096504016x14817158982636

Cited by 24 publications

(19 citation statements)

References 31 publications

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“…Previous studies have suggested an important role for DDX5 in regulating transcription in conjunction with multiple, sequence-specific transcription factors [21]. DDX5 is implicated in cancer development and progression by regulating cell proliferation, migration, cytoskeletal reorganization, and EMT [22][23][24][25][26]. DDX5 has been found to be involved in the oncogenic processes of osteosarcoma.…”

Section: Discussionmentioning

confidence: 99%

Long noncoding RNA DLEU1 aggravates osteosarcoma carcinogenesis via regulating the miR-671-5p/DDX5 axis

Chen

Zhang

Wang

2019

Artificial Cells, Nanomedicine, and Biotechnology

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Long non-coding RNAs (LncRNAs) have been proven to be involved in the progression of osteosarcoma. LncRNA DLEU1 was found to act as an oncogene in various types of cancer. In this study, we aimed to explore the biological functions of DLEU1 in osteosarcoma and the specific mechanism. Our results showed that DLEU1 was highly expressed in osteosarcoma tissue specimens and cells. Downregulation of DLEU1 in osteosarcoma cells inhibited the cell proliferation, migration and invasion. Further mechanistic analysis and functional assays demonstrated that DLEU1 exerted its role by sponging microRNA (miR)-671-5p in osteosarcoma cells. Moreover, DEAD-box helicase 5 (DDX5) was confirmed as the target of miR-671-5p. Furthermore, rescue assays indicated that miR-671-5p inhibitor significantly reversed the effects of DLEU1 knockdown on osteosarcoma cell proliferation and invasion while restoration of DDX5 rescued the proliferation and invasion of osteosarcoma cells transfected with miR-671-5p mimics. In conclusion, DLEU1 acted as an oncogene in osteosarcoma by directly sponging miR-671-5p and regulating the expression of DDX5. These findings suggested that DLEU1 might be a novel therapeutic target in the treatment of osteosarcoma. ARTICLE HISTORY

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Section: Discussionmentioning

confidence: 99%

Long noncoding RNA DLEU1 aggravates osteosarcoma carcinogenesis via regulating the miR-671-5p/DDX5 axis

Chen

Zhang

Wang

2019

Artificial Cells, Nanomedicine, and Biotechnology

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“…Mutation and overexpression of DDX5 are found in human cancers, and its overexpression predicts advanced clinical stage and poor survival in colorectal cancer (CRC) patients (25,26,27). Knockdown of DDX5 inhibited the proliferation of cancer cells in vitro and the growth of xenografts in immunodeficient hosts (28,29).…”

Section: Introductionmentioning

confidence: 99%

DDX5 promotes oncogene C3 and FABP1 expressions and drives intestinal inflammation and tumorigenesis

Abbasi

Long

et al. 2020

Life Sci. Alliance

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Tumorigenesis in different segments of the intestinal tract involves tissue-specific oncogenic drivers. In the colon, complement component 3 (C3) activation is a major contributor to inflammation and malignancies. By contrast, tumorigenesis in the small intestine involves fatty acid–binding protein 1 (FABP1). However, little is known of the upstream mechanisms driving their expressions in different segments of the intestinal tract. Here, we report that the RNA-binding protein DDX5 binds to the mRNA transcripts of C3 and Fabp1 to augment their expressions posttranscriptionally. Knocking out DDX5 in epithelial cells protected mice from intestinal tumorigenesis and dextran sodium sulfate (DSS)–induced colitis. Identification of DDX5 as a common upstream regulator of tissue-specific oncogenic molecules provides an excellent therapeutic target for intestinal diseases.

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“…Collectively, we proved that miR-1275 affected EC radiosensitivity by targeting WNT1-activated Wnt/β-catenin pathway, and similar mechanism was previously unearthed in the influence of miR-301a on the migration and radiosensitivity of EC cells. 43 More importantly, the rescue of WNT1 on miR-1275-regulated EC radiosensitivity was mediated by the enhancement of WNT1-regulated Wnt/β-catenin signalling per se on EMT, 44,45 thus indicating the strong association among miR-1275, EMT and WNT1 in regulating the radiosensitization of EC cells.…”

Section: Discussionmentioning

confidence: 96%

MicroRNA‐1275 induces radiosensitization in oesophageal cancer by regulating epithelial‐to‐mesenchymal transition via Wnt/β‐catenin pathway

Xie

You-yi

Fei

et al. 2019

J Cellular Molecular Medi

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Acquired radioresistance is one of the main obstacles for the anti‐tumour efficacy of radiotherapy in oesophageal cancer (EC). Recent studies have proposed microRNAs (miRNAs) as important participators in the development of radioresistance in various cancers. Here, we investigated the role of miR‐1275 in acquired radioresistance and epithelial‐mesenchymal transition (EMT) in EC. Firstly, a radioresistant cell line KYSE‐150R was established, with an interesting discovery was observed that miR‐1275 was down‐regulated in KYSE‐150R cells compared to the parental cells. Functionally, miR‐1275 inhibition elevated radioresistance in KYSE‐150 cells via promoting EMT, whereas enforced expression of miR‐1275 increased radiosensitivity in KYSE‐150R cells by inhibiting EMT. Mechanically, we demonstrated that miR‐1275 directly targeted WNT1 and therefore inactivated Wnt/β‐catenin signalling pathway in EC cells. Furthermore, WNT1 depletion countervailed the promoting effect of miR‐1275 suppression on KYSE‐150 cell radioresistance through hampering EMT, whereas WNT1 overexpression rescued miR‐1275 up‐regulation‐impaired EMT to reduce the sensitivity of KYSE‐150R cells to radiation. Collectively, our findings suggested that miR‐1275 suppressed EMT to encourage radiosensitivity in EC cells via targeting WNT1‐activated Wnt/β‐catenin signalling, providing a new therapeutic outlet for overcoming radioresistance of patients with EC.

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Knockdown of DDX5 Inhibits the Proliferation and Tumorigenesis in Esophageal Cancer

Cited by 24 publications

References 31 publications

Long noncoding RNA DLEU1 aggravates osteosarcoma carcinogenesis via regulating the miR-671-5p/DDX5 axis

Long noncoding RNA DLEU1 aggravates osteosarcoma carcinogenesis via regulating the miR-671-5p/DDX5 axis

DDX5 promotes oncogene C3 and FABP1 expressions and drives intestinal inflammation and tumorigenesis

MicroRNA‐1275 induces radiosensitization in oesophageal cancer by regulating epithelial‐to‐mesenchymal transition via Wnt/β‐catenin pathway

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