ArticleCancer cell international2021
Lnc-STYK1-2 regulates bladder cancer cell proliferation, migration, and invasion by targeting miR-146b-5p expression and AKT/STAT3/NF-kB signaling.
Article in Cancer cell international, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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11 citing papers in PubMed, 20 citations in OpenAlex.
- F7 Drives Gastric Cancer Metastasis Through Anoikis Resistance and Tumor Microenvironment Remodeling.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- From cell lines to the clinic: identifying a urinary BlCa-EV signature through comparative proteomics of bladder cancer lysates and extracellular vesicles.Cell communication and signaling : CCS · 2026Article
- STYK1 expression in breast cancer and its association with vascular invasion and clinicopathological features.Scientific reports · 2026Article
- Machine Learning Accurately Predicts Muscle Invasion of Bladder Cancer Based on Three miRNAs.Journal of cellular and molecular medicine · 2025Article
- The regulatory relationship between transcription factor STAT3 and noncoding RNA.Cellular & molecular biology letters · 2024Review
- DOCK8 interference alleviates Aβ‑induced damage of BV2 cells by inhibiting STAT3/NLRP3/NF‑κB signaling.Experimental and therapeutic medicine · 2023Article
- Circ_0001658 regulates PI3K/AKT signaling via the miR-671-5p/ITGA2 axis and affects the progress of papillary thyroid carcinoma.Annals of translational medicine · 2022Article
- NORAD-sponged miR-378c alleviates malignant behaviors of stomach adenocarcinoma via targeting NRP1.Cancer cell international · 2022Article
- The role of PI3K/AKT signaling pathway in gallbladder carcinoma.American journal of translational research · 2022Review
- Silencing circ‑BIRC6 inhibits the proliferation, invasion, migration and epithelial‑mesenchymal transition of bladder cancer cells by targeting the miR‑495‑3p/XBP1 signaling axis.Molecular medicine reports · 2021Article
- MIR100HG Regulates CALD1 Gene Expression by Targeting miR-142-5p to Affect the Progression of Bladder Cancer CellsFrontiers in molecular biosciences · 2021Article
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Authors and funding
8 authors at 4 institutions in 1 country.
Funding
Abstract
backgroundEpigenetic modulation by noncoding RNAs substantially contributes to human cancer development, but noncoding RNAs involvement in bladder cancer remains poorly understood. This study investigated the role of long noncoding RNA (lncRNA) lnc-STYK1-2 in tumorigenesis in cancerous bladder cells.
methodsDifferential lncRNA and mRNA profiles were characterized by high-throughput RNA sequencing combined with validation via quantitative PCR. Bladder cancer cell proliferation was assessed through MTS, and bladder cancer cell migration and invasion were assessed through a Transwell system. The in vivo tumorigenesis of bladder cancer cells was evaluated using the cancer cell line-based xenograft model. The dual-luciferase reporter assay verified the association of miR-146b-5p with lnc-STYK1-2 and the target gene. Protein abundances and phosphorylation were detected by Western blotting.
resultsAlterations in lncRNA profiles, including decreased lnc-STYK1-2 expression, were detected in bladder cancer tissues compared with adjacent noncancerous tissues. lnc-STYK1-2 silencing effectively promoted proliferation, migration, and invasion in two bladder cancer cell lines, 5637 and T24, and their tumorigenesis in nude mice. lnc-STYK1-2 siRNA promoted miR-146b-5p and reduced ITGA2 expression in bladder cancer cells. Moreover, miR-146b-5p suppressed ITGA2 expression in bladder cancer cells through direct association. Also, lnc-STYK1-2 directly associated with miR-146b-5p. Finally, miR-146b-5p inhibitors abrogated the alterations in bladder cell functions, ITGA2 expression, and phosphorylation of AKT, STAT3, and P65 proteins in 5637 and T24 cells induced by lnc-STYK1-2 silencing.
conclusionlnc-STYK1-2 inhibited bladder cancer cell proliferation, migration, and tumorigenesis by targeting miR-146b-5p to regulate ITGA2 expression and AKT/STAT3/NF-kB signaling.
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