Long Noncoding RNA LINC02470 Sponges MicroRNA-143-3p and Enhances SMAD3-Mediated Epithelial-to-Mesenchymal Transition to Promote the Aggressive Properties of Bladder Cancer

Huang, Chengshuo; Tsai, Chin-Ho; Yu, Cheng; Wu, Ying-Si; Yee, Ming-Fong; Ho, Jar-Yi; Yü, Dah‐Shyong

doi:10.3390/cancers14040968

Cited by 14 publications

(9 citation statements)

References 65 publications

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“…The prostate cancer progression was activated when the SMAD3 was upregulated [ 27 ]. SMAD3 could activate the TGF-β-induced EMT process of bladder cancer cells [ 28 ]. We can also observe that SMAD3 can promote the cancer progression, as demonstrated in this study.…”

Section: Discussionmentioning

confidence: 99%

RAB26 contributes to the progression of non-small cell lung cancer after being transcriptionally activated by SMAD3

Ren

Yang

et al. 2022

Bioengineered

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Non-small cell lung cancer (NSCLC) accounts for 85% of all cases of lung cancer, which constitutes the leading cause of cancer mortality. RAB26, a member of Rab GTPase superfamily, has been suggested to play a role in the tumorigenesis of NSCLC. The present work aimed to explore whether and how RAB26 contributed to the progression of NSCLC. NSCLC cell line A549 was transfection with short hairpin RNA (shRNA) or overexpression (Ov) vector to knockdown RAB26 or overexpress SMAD3, respectively. Then the malignant processes of A549 cells including proliferation, migration, invasion and apoptosis were evaluated by CCK-8, colony formation, wound-healing, transwell and TUNEL assays, respectively. Expression of proteins involved in these processes was measured by western blot. A549 xenograft mice model was established to confirm the effect of RAB26 silence on NSCLC progression in vivo. The relationship between RAB26 and SMAD3 was analyzed by bioinformatics and then verified by dual-luciferase reporter and chromatin immunoprecipitation (ChIP) assays. We found that silence of RAB26 inhibited the proliferation, migration and invasion but promoted apoptosis of A549 cells. In vivo studies revealed that the tumor growth of A549 xenograft was markedly suppressed upon RAB26 silence. Moreover, it was confirmed that SMAD3 bound to the promoter of RAB26 and enhance its expression. Finally, we observed that overexpression of SMAD3 significantly blocked the inhibitory effect of RAB26 silence on NSCLC progression. Collectively, RAB26 may contribute to the progression of NSCLC after being transcriptionally activated by SMAD3.

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Section: Discussionmentioning

confidence: 99%

RAB26 contributes to the progression of non-small cell lung cancer after being transcriptionally activated by SMAD3

Ren

Yang

et al. 2022

Bioengineered

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“…These results may explain the poor prognosis of patients with high AIGS. Notably, studies have shown that the E2F targets pathway is associated with chemotherapy resistance in bladder cancer [ 40 ]. Combined with the results of GSVA, patients with low AIGS may be more sensitive to chemotherapy, which paralleled our result in GSE52219 .…”

Section: Discussionmentioning

confidence: 99%

Artificial intelligence‐driven consensus gene signatures for improving bladder cancer clinical outcomes identified by multi‐center integration analysis

Liu

Weng

et al. 2022

Molecular Oncology

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To accurately predict the prognosis and further improve the clinical outcomes of bladder cancer (BLCA), we leveraged large-scale data to develop and validate a robust signature consisting of small gene sets. Ten machine-learning algorithms were enrolled and subsequently transformed into 76 combinations, which were further performed on eight independent cohorts (n = 1218). We ultimately determined a consensus artificial intelligence-derived gene signature (AIGS) with the best performance among 76 model types. In this model, patients with high AIGS showed a higher risk of mortality, recurrence, and disease progression. AIGS is not only independent of traditional clinical traits [(e.g., American Joint Committee on Cancer (AJCC) stage)] and molecular features (e.g., TP53 mutation) but also demonstrated superior performance to these variables. Comparisons with 58 published signatures also indicated that AIGS possessed the best performance. Additionally, the combination of AIGS and AJCC stage could achieve better performance. Patients with low AIGS scores were sensitive to immunotherapy, whereas patients with high AIGS scores might benefit from seven potential therapeutics: BRD-K45681478, 1S,3R-RSL-3, RITA, U-0126, temsirolimus, MRS-1220, and LY2784544. Additionally, some mutations (TP53 and RB1), copy number variations (7p11.2), and a methylation-driven target were characterized by AIGS-related multi-omics alterations. Overall, AIGS provides an attractive platform to optimize decision-making and surveillance protocol for individual BLCA patients.

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“…In addition, the E2F4 TF was critical to repress MIR497HG transcription in BC cells. On the other hand, Linc02470 was identified in the lnCAR database as one of the most upregulated lncRNAs expressed during BC initiation and progression ( 84 ). In the context of TGF-β signaling, Linc02470 directly targeted the miR-143-3p , promoting SMAD3 expression, which consequently induced SNAI1, SNAI2, ZEB2, vimentin, and N-cadherin expression.…”

Section: Bladder Cancermentioning

confidence: 99%

Unboxing the network among long non-coding RNAs and TGF-β signaling in cancer

Rodrigues-Junior,

Moustakas

2024

ujms

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Deeper analysis of molecular mechanisms arising in tumor cells is an unmet need to provide new diagnostic and therapeutic strategies to prevent and treat tumors. The transforming growth factor β (TGF-β) signaling has been steadily featured in tumor biology and linked to poor prognosis of cancer patients. One pro-tumorigenic mechanism induced by TGF-β is the epithelial-to-mesenchymal transition (EMT), which can initiate cancer dissemination, enrich the tumor stem cell population, and increase chemoresistance. TGF-β signals via SMAD proteins, ubiquitin ligases, and protein kinases and modulates the expression of protein-coding and non-coding RNA genes, including those encoding larger than 500 nt transcripts, defined as long non-coding RNAs (lncRNAs). Several reports have shown lncRNAs regulating malignant phenotypes by directly affecting epigenetic processes, transcription, and post-transcriptional regulation. Thus, this review aims to update and summarize the impact of TGF-β signaling on the expression of lncRNAs and the function of such lncRNAs as regulators of TGF-β signaling, and how these networks might impact specific hallmarks of cancer.

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Long Noncoding RNA LINC02470 Sponges MicroRNA-143-3p and Enhances SMAD3-Mediated Epithelial-to-Mesenchymal Transition to Promote the Aggressive Properties of Bladder Cancer

Cited by 14 publications

References 65 publications

RAB26 contributes to the progression of non-small cell lung cancer after being transcriptionally activated by SMAD3

RAB26 contributes to the progression of non-small cell lung cancer after being transcriptionally activated by SMAD3

Artificial intelligence‐driven consensus gene signatures for improving bladder cancer clinical outcomes identified by multi‐center integration analysis

Unboxing the network among long non-coding RNAs and TGF-β signaling in cancer

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