ArticleMolecular therapy oncolytics2019
OCT4B1 Promoted EMT and Regulated the Self-Renewal of CSCs in CRC: Effects Associated with the Balance of miR-8064/PLK1.
Article in Molecular therapy oncolytics, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 23 citations in OpenAlex.
- Overexpression of oncogenic polo-like kinase 1 disrupts the invasiveness, cell cycle, and apoptosis in synovial sarcoma.Journal of translational medicine · 2025Article
- OCT4 and MENA immunoprofiling in salivary mucoepidermoid carcinoma.Diagnostic pathology · 2025Article
- Review
- Pseudogene OCT4-pg5 upregulates OCT4B expression to promote bladder cancer progression by competing with miR-145-5p.Cell cycle (Georgetown, Tex.) · 2024Article
- Role of stemness-related genes TIMP1, PGF, and SNAI1 in the prognosis of colorectal cancer through single-cell RNA-seq.Cancer medicine · 2023Article
- Expression ofFrontiers in oncology · 2023Article
- Article
- Discovery of a tetrahydroisoquinoline-based CDK9-cyclin T1 protein-protein interaction inhibitor as an anti-proliferative and anti-migration agent against triple-negative breast cancer cells.Genes & diseases · 2022Article
- Ectopic expression of OCT4B1 Decreases Fertility Rate and Changes Sperm Parameters in Transgenic Mice.Iranian journal of biotechnology · 2022Article
- ANGPTL1 attenuates cancer migration, invasion, and stemness through regulating FOXO3a-mediated SOX2 expression in colorectal cancer.Clinical science (London, England : 1979) · 2022Article
- Emodin exerts antitumor effects in ovarian cancer cell lines by preventing the development of cancer stem cells via epithelial mesenchymal transition.Oncology letters · 2022Article
- Generation of Mesenchymal Cell Lines Derived from Aged Donors.International journal of molecular sciences · 2021Article
- MicroRNA‑8063 targets heterogeneous nuclear ribonucleoprotein AB to inhibit the self‑renewal of colorectal cancer stem cells via the Wnt/β‑catenin pathway.Oncology reports · 2021Article
- LAT1 and ASCT2 Related microRNAs as Potential New Therapeutic Agents against Colorectal Cancer Progression.Biomedicines · 2021Review
- EMT and Cancer Cell Stemness Associated With Chemotherapeutic Resistance in Esophageal Cancer.Frontiers in oncology · 2021Article
- A Pilot Study Investigating the Expression Levels of Pluripotency-Associated Genes in Rectal Swab Samples for Colorectal Polyp and Cancer Diagnosis and Prognosis.Stem cells international · 2021Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cancer stem cells (CSCs) are the main cause of tumor generation, recurrence, metastasis, and therapy failure in various malignancies including colorectal cancer (CRC). Accumulating evidence suggests that tumor cells can acquire CSC characteristics through the epithelial-mesenchymal transition (EMT) process. However, the molecular mechanism of CSCs remains unclear. OCT4B1 is a transcript of OCT4, which is initially expressed in embryonic stem and carcinoma cells, and is involved in the regulation and maintenance of an undifferentiated state of stem cells. In this study, three-dimensional (3D) microspheres were confirmed as CRC stem cells. Compared with that of parental cells, their self-renewal ability was significantly increased, and OCT4B1 expression was increased and promoted the EMT process. The knockdown of OCT4B1 decreased the self-renewal of CSCs and reversed EMT. Moreover, OCT4B1 induced the expression of Polo-like kinase 1 (PLK1), which is a key regulator of EMT in tumor cells. Further examination showed that OCT4B1 regulated the miR-8064/PLK1 balance to exert its function. Taken together, our data suggest that OCT4B1 may be involved in regulating the self-renewal of colorectal CSCs through EMT, which is at least partially due to the miR-8064/PLK1 balance. This study indicates that OCT4B1 is a potential therapeutic target for CRC by targeting CSCs.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.