RETRACTED ARTICLE: MicroRNA-338-3p suppresses ovarian cancer cells growth and metastasis: implication of Wnt/catenin beta and MEK/ERK signaling pathways

Zhang, Ruitao; Shi, Huirong; Ren, Fang; Feng, Wen; Cao, Yuan; Li, Gailing; Liu, Zheying; Ji, Pengcheng; Zhang, Minghui

doi:10.1186/s13046-019-1494-3

Cited by 58 publications

(50 citation statements)

References 50 publications

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“…Then, we predicted the potential miRNAs that bind to circ_0038467 using the online database Circinteractome and validated that circ_0038467 acted as a sponge of miR‐338‐3p in 16HBE cells. MiR‐338‐3p has been reported to repress tumorigenesis and progression of multiple human tumors, such as ovarian cancer, gastric cancer and NSCLC . MiR‐338‐3p was also demonstrated to be downregulated in acute kidney injury .…”

Section: Discussionmentioning

confidence: 99%

Circ_0038467 regulates lipopolysaccharide‐induced inflammatory injury in human bronchial epithelial cells through sponging miR‐338‐3p

Liu

Wan

et al. 2020

Thoracic Cancer

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Background: Pneumonia is a common acute lower respiratory infection in children and elders. Circular RNAs (circRNAs) have recently been uncovered to play important roles in pneumonia. However, the function and mechanism of circ_0038467 in pneumonia remain elusive. Methods: Cell viability and apoptosis were determined using the Cell Counting Kit-8 (CCK-8) assay and flow cytometry, respectively. The levels of interleukin 6 (IL-6), IL-8 and IL-1β were detected by enzyme-linked immunosorbent assay (ELISA). Western blot analysis was performed to assess the expression of related proteins. Circ_0038467 was characterized by Ribonuclease R (RNase) digestion and subcellular localization assays. The levels of circ_0038467 and miR-338-3p were evaluated by quantitative real-time polymerase chain reaction (qRT-PCR). The direct interaction between circ_0038467 and miR-338-3p was validated by the dual-luciferase reporter and RNA immunoprecipitation (RIP) assays. Results: Our data indicated that lipopolysaccharide (LPS) induced an inflammatory injury in 16HBE cells by repressing cell viability and enhancing cell apoptosis and proinflammatory cytokines production. Circ_0038467 was upregulated and miR-338-3p was downregulated in LPS-treated 16HBE cells. Circ_0038467 knockdown or miR-338-3p overexpression attenuated LPS-induced 16HBE cell inflammatory injury. Moreover, circ_0038467 acted as a sponge of miR-338-3p in 16HBE cells. MiR-338-3p mediated the alleviated effect of circ_0038467 knockdown on LPS-induced 16HBE cell inflammatory injury. Additionally, the Janus kinase/ signal transducer and activator of transcription 3 (JAK/STAT3) signaling pathway was involved in the circ_0038467/miR-338-3p axis-mediated regulation in LPS-induced 16HBE cell inflammatory injury. Conclusions: The current work had led to the identification of circ_0038467 knockdown that alleviated LPS-induced inflammatory injury in 16HBE cells at least partly through sponging miR-338-3p and regulating JAK/STAT3 pathway, highlighting novel molecular targets for the treatment of pneumonia.

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Section: Discussionmentioning

confidence: 99%

Circ_0038467 regulates lipopolysaccharide‐induced inflammatory injury in human bronchial epithelial cells through sponging miR‐338‐3p

Liu

Wan

et al. 2020

Thoracic Cancer

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“…Tumor cell invasion and migration are multistep processes which are nely regulated [20][21][22]. The epithelial-to-mesenchymal transition (EMT) has been identi ed as an important process of tumor cell invasion and migration [23][24][25]. Therefore, we determined the effects of PNN on EMT in prostate cancer cell.…”

Section: Pnn Over-expression Induces Prostate Cancer Cell Emtmentioning

confidence: 99%

Pinin promotes tumor progression via PI3K/AKT/CREB signaling pathway in prostate cancer

Meng

Zhang²,

Ren

et al. 2020

Preprint

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Abstract Background Pinin (PNN), a desmosome associated protein, was demonstrated to be over-expressed and act as a tumor-promoting factor in ovarian cancer, hepatocellular carcinoma and colorectal cancer. However, the precise role of PNN in prostate cancer is still unknown. Methods The expression levels of PNN were assessed in prostate cancer by qRT-PCR, western blotting and immunohistochemical staining. The other proteins were quantified by western blotting. PNN-depleted cells were produced by infecting with lentivirus bearing short hairpin RNAs against PNN. PNN over-expression was performed by transfecting PNN expression vector. The proliferation of each cell line was assessed by MTS and colony formation assays. Tumors were induced on nude mice by injecting tumor cells subcutaneously. Apoptosis and cell cycle were evaluated by flow cytometry. Transwell and wound healing assay were performed to determined the ability of cell invasion and migration. The TCGA data were analyzed with GEPIA (Gene Expression Profiling Interactive Analysis) and GraphPad Prism. Results Here, we reported that PNN was upregulated in prostate cancer tissues and PNN expression was positively associated with Gleason score, tumor stage and tumor metastasis. PNN promoted cell growth and tumorigenicity in vitro and in vivo, and might modulate cell growth through driving G1/S transition via CDK6, CDK2, and Cyclin D1 in prostate cancer cells. Furthermore, PNN accelerated cell invasion, migration and EMT processes of prostate cancer cells accompanied with the up-regulation of MMP-2, MMP-9, N-cadherin, Vimentin and down-regulation of E-cadherin. Mechanism study demonstrated that the proliferation- and motility-promoting effects of PNN on prostate cancer cells dependent on the activation of PI3K/AKT/CREB signaling, which was reversed by AKT and CREB inhibitors. Conclusions Collectively, these findings indicated that PNN plays important roles in prostate cancer tumorigenesis and progression and it may be a potential therapeutic target for prostate cancer treatment.

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“…Previous studies have shown that miR-338 could suppress tumor progression in various human cancers. Zhang et al found that miR-338 inhibited bladder cancer cell proliferation and invasion by reducing ETS1 [23]. He et al con rmed that miR-338 inhibited cell proliferation and the expression of EMT markers of NSCLC cells by directly downregulating the NFATc1 expression [24].…”

Section: Discussionmentioning

confidence: 99%

circRAE1 promotes colorectal cancer cell migration and invasion through modulating miR-338-3p/TYRO3 axis

Chen

et al. 2020

Preprint

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Background: Growing evidences have revealed that long non-coding RNAs (lncRNAs) including circular RNAs (circRNAs) involve in numerous carcinogenesis. However, the roles of circRNAs in the cancer biology of colorectal cancer (CRC) remain vague. Methods: qRT-PCR and western-blot were used to detecte the circRAE1 levels in CRC tissues and CRC cell lines.,Cell proliferation, migration and invasion were detected using wound healing assays, and transwell assays. The interaction between circRAE1 and miR-338-3p and TRYO3 was confirmed by dual-luciferase reporter assays. Results: We uncovered that a novel circRNA Hsa_circ_0060967 (also known as circRAE1) was remarkably increased in CRC tissues, and high circRAE1 level was positively associated with advanced tumor stage, lymph node metastasis, and tumor size. Loss-of-function assay indicated that circRAE1 accelerated cell proliferation, migration and invasion. Besides, miR-338-3p , lowly expressed in CRC tissues and CRC cell lines. dual-luciferase reporter assays showed that circRAE1 could sponge miR-338-3p, which targeted TRYO3 in CRC cells. Furthermore, overexpression of circRAE1 could recue the impaired migration and invasion triggered by miR-338-3p mimics or si-TYRO3 in CRC cells and vice versa. Conclusion : we figured out the network of circRAE1, miR-338-3p, and TYRO3 in CRC cells and revealed that increased circRAE1 served as an oncogene through sponging miR-338-3p, resulting in upregulated TYRO3 expression, which suggested that circRAE1 would be a potential therapeutic target and diagnostic marker for CRC treatment.

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RETRACTED ARTICLE: MicroRNA-338-3p suppresses ovarian cancer cells growth and metastasis: implication of Wnt/catenin beta and MEK/ERK signaling pathways

Cited by 58 publications

References 50 publications

Circ_0038467 regulates lipopolysaccharide‐induced inflammatory injury in human bronchial epithelial cells through sponging miR‐338‐3p

Circ_0038467 regulates lipopolysaccharide‐induced inflammatory injury in human bronchial epithelial cells through sponging miR‐338‐3p

Pinin promotes tumor progression via PI3K/AKT/CREB signaling pathway in prostate cancer

circRAE1 promotes colorectal cancer cell migration and invasion through modulating miR-338-3p/TYRO3 axis

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