<i>Retracted:</i> Reduced levels of miR‐485‐5p in HPV‐infected cervical cancer promote cell proliferation and enhance invasion ability

Dai, Yuanyuan; Xie, Fengyan; Yan, Chen

doi:10.1002/2211-5463.12869

Cited by 9 publications

(4 citation statements)

References 33 publications

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“…A previous study showed that miR‐485‐5p suppressed the invasion of cancer cells by targeting FLOT‐1 in HPV‐infected cervical carcinoma cells 24 . Another study showed that elevated expression of miR‐485‐3p suppressed ki‐67 and cyclin D1 expression in NSCs.…”

Section: Discussionmentioning

confidence: 99%

MiR-485 targets the DTX4 gene to regulate milk fat synthesis in bovine mammary epithelial cells

Liu

Ping

Iqbal

et al. 2021

Sci Rep

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MicroRNAs (miRNAs) are mRNA suppressors that regulate a variety of cellular and physiological processes, including cell proliferation, apoptosis, triglyceride synthesis, fat formation, and lipolysis, by post-transcriptional processing. In previous studies, we isolated and sequenced miRNAs from mammary epithelial cells from Chinese Holstein cows with high and low milk fat percentages. MiR-485 was one of the significantly differentially expressed miRNAs that were identified. In the present study, the relationship between the candidate target gene DTX4 and miR-485 was validated by bioinformatics and real-time fluorescent quantitative PCR (qRT-PCR) and Western blot (WB) analyses in bovine mammary epithelial cells (bMECs). The results indicated that miR-485 negatively regulated the mRNA expression of the target gene DTX4. Furthermore, an shRNA interference vector for the target gene DTX4 was constructed successfully, and it increased the triglyceride content and reduced the cholesterol content of transfected cells. These results suggest that miR-485 may affect the contents of triglycerides (TGs) and cholesterol (CHOL) by targeting the DTX4 gene. This study indicates that miR-485 has a role in regulating milk fat synthesis and that miR-485 targets the DTX4 gene to regulate lipid metabolism in bMECs. These findings contribute to the understanding of the functional significance of miR-485 in milk fat synthesis.

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Section: Discussionmentioning

confidence: 99%

MiR-485 targets the DTX4 gene to regulate milk fat synthesis in bovine mammary epithelial cells

Liu

Ping

Iqbal

et al. 2021

Sci Rep

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“…It inhibited breast cancer progression and chemoresistance through targeting surviving ( Wang et al, 2018a , Wang et al, 2018b ) or MUC1 ( Wang et al, 2020 ). Reduction in miR-485-5p expression in HPV-infected cervical cancer led to an increase in cell proliferation and invasion ( Dai et al, 2020 ). As for in OC, miR-485-5p was found to be poorly expressed in tumors and associated with disease grade ( Kim et al, 2010 ), and as aforementioned, to increase chemosensitivity of OC cells ( Qiao et al, 2020 ).…”

Section: Discussionmentioning

confidence: 99%

E74-like factor 3 suppresses microRNA-485-5p transcription to trigger growth and metastasis of ovarian cancer cells with the involvement of CLDN4/Wnt/β-catenin axis

Kuang

2021

Saudi Journal of Biological Sciences

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Ovarian cancer (OC) is one of the most prevailing gynecological malignancies with high mortality rate, while E74 like ETS transcription factor 3 (ELF3) is reported to be associated with tumorigenesis. This work aims to analyze the role of ELF3 on the suppression of miR-485-5p transcription in OC. Expression of ELF3 in OC and its correlation with overall survival were predicted on a bioinformation system GEPIA. Then, the level of ELF3 in OC tissues and cells and in normal ones was evaluated. Binding relationships between ELF3 and microRNA (miR)-485-5p, and between miR-485-5p and claudin-4 (CLND4) were predicted through Bioinformatics tools. Altered expression of ELF3, miR-485-5p and CLND4 was introduced alone or jointly to probe their influences on OC cell growth. ELF3 was suggested to be highly expressed in OC, which was linked to poor prognosis in patients. Abundant expression of ELF3 was identified in OC tissues and cell lines as relative to the normal ones. ELF3 inhibition suppressed growth and metastasis of OC cells. ELF3 transcriptionally suppressed miR-485-5p expression to further enhance CLDN4 expression. Overexpression of miR-485-5p led to similar trends as ELF3 inhibition did. Importantly, upregulation of CLDN4 was found to block the roles of ELF3 inhibition in OC cells. In addition, the Wnt/signaling pathway suppressed by miR-485-5p mimic was reactivated following CLDN4 overexpression. This study evidenced that ELF3 suppresses miR-485-5p transcription to enhance CLDN4 expression, leading to Wnt/β-catenin activation and promoting OC cell growth and metastasis. This work may provide new ideas for gene-based therapies for OC.

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“…According to our online prediction, there is a binding relationship between LINC01419, miR‐485‐5p, and LSM4. The regulation of miR‐485‐5p on various malignant tumors, such as cervical cancer (CC), 13 renal cell carcinoma, 14 and gastric cancer (GC) 15 has been reported. More importantly, miR‐485‐5p is widely accepted as a tumor suppressor in HCC, 16,17 and its effects on the regulation of HCC cell biological activities can be restrained by lncRNAs through epigenetic regulation 18,19 .…”

Section: Introductionmentioning

confidence: 99%

Long noncoding RNA LINC01419 promotes hepatocellular carcinoma malignancy by mediating miR‐485‐5p/LSM4 axis

Sun

Tan

Peng

2022

The Kaohsiung J of Med Scie

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To investigate the effect of long noncoding RNA (LINC01419)/miR‐485‐5p/LSM4 on the malignant behavior of hepatocellular carcinoma (HCC) cells. The expressions of LINC01419, miR‐485‐5p, and LSM4 were determined in HCC at the cellular and clinical levels, and cell biological behavior was evaluated. The relationships between LINC01419, miR‐485‐5p, and LSM4 were predicted and verified. Additionally, the subcellular localization of LINC01419 in HCC cells was analyzed. Finally, an animal experiment was conducted to confirm the effect of LINC01419 silencing on tumor growth. in HCC tissues and cells, LINC01419 and LSM4 were increasingly expressed, but miR‐485‐5p was decreasingly expressed. LINC01419 negatively regulated miR‐485‐5p‐ and miR‐485‐5p‐targeted LSM4. LINC01419 was localized in the cytoplasm of HCC cells. Downregulation of miR‐485‐5p or upregulation of LSM4 reversed the inhibition of HCC cell malignant behavior by LINC01419 interference. LINC01419 sponges miR‐485‐5p to upregulate LSM4 expression, thereby facilitating the biological behavior of HCC cells.

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Retracted: Reduced levels of miR‐485‐5p in HPV‐infected cervical cancer promote cell proliferation and enhance invasion ability

Cited by 9 publications

References 33 publications

MiR-485 targets the DTX4 gene to regulate milk fat synthesis in bovine mammary epithelial cells

MiR-485 targets the DTX4 gene to regulate milk fat synthesis in bovine mammary epithelial cells

E74-like factor 3 suppresses microRNA-485-5p transcription to trigger growth and metastasis of ovarian cancer cells with the involvement of CLDN4/Wnt/β-catenin axis

Long noncoding RNA LINC01419 promotes hepatocellular carcinoma malignancy by mediating miR‐485‐5p/LSM4 axis

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