<i>Retracted</i>: MicroRNA‐4429 restrains colorectal cancer cell invasion and migration via regulating SMAD3‐induced epithelial–mesenchymal transition

Li, Hongwen; Liang, Weijie; Zhang, Hongyu; Shui, Yifang; Zhang, Zhe

doi:10.1002/jcp.30271

Cited by 9 publications

(5 citation statements)

References 36 publications

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“…SMAD4 is a tumor suppressor gene that plays a central role in TGF-β signaling pathway transduction [25]. In CRC, SMAD3 reduces its expression through miR-4429 and ultimately inhibits the occurrence, development, and metastasis of cancer cells [26]. A meta-analysis showed that a high mutation rate of SMAD4 in CRC patients was associated with poor prognosis but not with clinical stage [27].…”

Section: Discussionmentioning

confidence: 99%

Correlation between SMADs and Colorectal Cancer Expression, Prognosis, and Immune Infiltrates

Ding

Luo

et al. 2023

International Journal of Analytical Chemistry

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Background. In recent years, the incidence and mortality of colorectal cancer (CRC) are increasing, and the 5-year survival rate of advanced metastatic CRC is poor. Small mothers against decapentaplegic (SMAD) superfamily are intracellular signal transduction proteins associated with the development and prognosis of a variety of tumors. At present, no study has systematically analysed the relationship between SMADs and CRC. Methods. Here, R3.6.3 was used to analyse the expression of SMADs in pan-cancer and CRC. Protein expression of SMADs were analysed by Human Protein Atlas (HPA). Gene expression profiling interactive analysis (GEPIA) was used to evaluate the correlation between SMADs and tumor stage in CRC. The effect of R language and GEPIA on prognosis was analysed. Mutation rates of SMADs in CRC were determined by cBioPortal, and potentially related genes were predicted using GeneMANIA. R analysis was used to correlate immune cell infiltration in CRC. Results. Both SMAD1 and SMAD2 were found to be weakly expressed in CRC and correlated with the immune invasion level. SMAD1 was correlated with patient prognosis, and SMAD2 was correlated with tumor stage. SMAD3, SMAD4, and SMAD7 were all expressed at low levels in CRC and associated with a variety of immune cells. SMAD3 and SMAD4 proteins were also expressed at low levels, and SMAD4 had the highest mutation rate. SMAD5 and SMAD6 were overexpressed in CRC, and SMAD6 was also associated with patient overall survival (OS) and CD8+ T cells, macrophages, and neutrophils. Conclusions. Our results reveal innovative and strong evidence that SMADs can be used as biomarkers for the treatment and prognosis of CRC.

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Section: Discussionmentioning

confidence: 99%

Correlation between SMADs and Colorectal Cancer Expression, Prognosis, and Immune Infiltrates

Ding

Luo

et al. 2023

International Journal of Analytical Chemistry

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“…Smad3 plays important roles in the cell proliferation, invasion and metastasis of cancer cells, such as lung cancer ( 41 ), colorectal cancer ( 42 ), and chordoma ( 43 ). TGF-β could promote the progression of tumorigenesis in BC and facilitate cancer cell migration and invasion through the Smad3 signaling pathway ( 44 ).…”

Section: Discussionmentioning

confidence: 99%

WFDC21P promotes triple-negative breast cancer proliferation and migration through WFDC21P/miR-628/SMAD3 axis

et al. 2022

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Long non-coding RNAs (lncRNAs) modulate cell proliferation, cycle, and apoptosis. However, the role of lncRNA-WFDC21P in the tumorigenesis of triple-negative breast cancer (TNBC) remains unclear. Results of this study demonstrated that WFDC21P levels significantly increased in TNBC, which was associated with the poor survival of patients. WFDC21P overexpression significantly promoted TNBC cell proliferation and metastasis. WFDC21P interacted with miR-628-5p, which further suppressed cell proliferation and metastasis by negatively regulating Smad3-related gene expression. Recovery of miR-628-5p weakened the roles of WFDC21P in promoting the growth and metastasis of TNBC cells. Moreover,N6-methyladenosine (m6A) modification upregulated WFDC21P expression in the TNBC cells. WFDC21P and its m6A levels were increased after methyltransferase like 3 (METTL3) overexpression but reduced after METTL3 silencing. The proliferation and metastasis of TNBC cells were promoted by METTL3 overexpression but suppressed by METTL3 silencing. This study demonstrated the vital roles of WFDC21P and its m6A in regulating the proliferation and metastasis of TNBC cells via the WFDC21P/miR-628/SMAD3 axis.

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“…Wang et al ( 33 ) found that miR-4429 inhibits the growth of prostate cancer cells by downregulating DLX1 and inactivating the Wnt/β-catenin pathway. Li et al ( 34 ) demonstrated that miR-4429 blocks the proliferation, migration, invasion and epithelial-mesenchymal transition (EMT) process of CRC cells by targeting FOXM1 to downregulate SMAD3. Cai et al ( 35 ) confirm that the silencing of lncRNA SNHG12 and overexpression of miR-4429 significantly inhibit the proliferation, migration and invasion of RL95-2 cells by downregulating MMP2 and MMP9 and targeting of the SNHG12/miR-4429 axis and can be used as a potential therapeutic target for endometrial cancer in the future.…”

Section: Discussionmentioning

confidence: 99%

Overexpressed lncRNA FTX promotes the cell viability, proliferation, migration and invasion of renal cell carcinoma via FTX/miR‑4429/UBE2C axis

Chen

Zhang

et al. 2022

Oncol Rep

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The present study aimed to explore the role of long non-coding (lnc)RNA FTX and ubiquitin-conjugating enzyme E2C (UBE2C) in promoting the progression of renal cell carcinoma (RCC) and the underlying regulatory mechanism. Relative levels of lncRNA FTX, UBE2C, AKT, CDK1 and CDK6 in RCC cell lines were detected by reverse transcription-quantitative (RT-q). Expression levels of UBE2C, phosphorylated (p)-AKT/AKT, p-CDK1/CDK1 and p-CDK6/CDK6 in RCC and paracancerous specimens and RCC cells were measured by western blot or immunohistochemistry assay. In addition, the proliferative rate, cell viability, cell cycle progression, migratory rate and invasive rate of RCC cells overexpressing lncRNA FTX by lentivirus transfection were determined by a series of functional experiments, including the colony formation assay, MTT assay, flow cytometry, Transwell assay and wound healing assay. The targeted binding relationship in the lncRNA FTX/miR-4429/UBE2C axis was validated by dual-luciferase reporter assay. By intervening microRNA (miR)-4492 and UBE2C by the transfection of miR-4429-mimics or short interfering UBE2C-2, the regulatory effect of lncRNA FTX/miR-4429/UBE2C axis on the progression of RCC was evaluated. Finally, a xenograft model of RCC in nude mice was established by subcutaneous implantation, thus evaluating the in vivo function of lncRNA FTX in the progression of RCC. The results showed that lncRNA FTX and UBE2C were upregulated in RCC specimens and cell lines. The overexpression of lncRNA FTX in RCC cells upregulated UBE2C. In addition, the overexpression of lncRNA FTX promoted the cell viability and proliferative, migratory and invasive capacities of RCC cells and accelerated the cell cycle progression. A dual-luciferase reporter assay validated that lncRNA FTX exerted the miRNA sponge effect on miR-4429, which was bound to UBE2C 3'UTR. Knockdown of UBE2C effectively reversed the regulatory effects of overexpressed lncRNA FTX on the abovementioned phenotypes of RCC cells. In the xenograft model of RCC, the mice implanted with RCC cells overexpressing lncRNA FTX showed a larger tumor size and higher tumor weight than those of controls, while the in vivo knockdown of UBE2C significantly reduced the size of RCC lesions, indicating the reversed cancer-promoting effect of lncRNA FTX. Overall, the present study showed that lncRNA FTX was upregulated in RCC and could significantly promote the proliferative, migratory and invasive capacities, enhancing the viability and accelerating the cell cycle progression of RCC cells by exerting the miRNA sponge effect on miR-4429 and thus upregulating UBE2C. lncRNA FTX and UBE2C are potential molecular biomarkers and therapeutic targets of RCC.

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Retracted: MicroRNA‐4429 restrains colorectal cancer cell invasion and migration via regulating SMAD3‐induced epithelial–mesenchymal transition

Cited by 9 publications

References 36 publications

Correlation between SMADs and Colorectal Cancer Expression, Prognosis, and Immune Infiltrates

Correlation between SMADs and Colorectal Cancer Expression, Prognosis, and Immune Infiltrates

WFDC21P promotes triple-negative breast cancer proliferation and migration through WFDC21P/miR-628/SMAD3 axis

Overexpressed lncRNA FTX promotes the cell viability, proliferation, migration and invasion of renal cell carcinoma via FTX/miR‑4429/UBE2C axis

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