ArticleDrug design, development and therapy2020
Regulations of miR-183-5p and Snail-Mediated Shikonin-Reduced Epithelial-Mesenchymal Transition in Cervical Cancer Cells.
Article in Drug design, development and therapy, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 28 citations in OpenAlex.
- Shikonin inhibits epithelial-mesenchymal transition in glioblastoma cells by upregulating p53 and promoting miR-361-5p level to suppress ZEB1 expression.BMC neuroscience · 2025Article
- Drug-containing Serum of Quyoufang Promotes Apoptosis of Ectocervical H8 Cells through an E6/p53-related Pathway.Combinatorial chemistry & high throughput screening · 2025Article
- Review projecting shikonin as a therapeutic candidate in female carcinomas: a preclinical perspective.Frontiers in pharmacology · 2025Review
- Serinc2 Drives the Progression of Cervical Cancer Through Regulating Myc Pathway.Cancer medicine · 2024Article
- Extracellular vesicles derived from paclitaxel-sensitive nasopharyngeal carcinoma cells deliver miR-183-5p and impart paclitaxel sensitivity through a mechanism involving P-gp.Cell biology and toxicology · 2023Article
- Review
- Shikonin inhibits the proliferation of cervical cancer cells via FAK/AKT/GSK3β signalling.Oncology letters · 2022Article
- Article
- DYNLT3 overexpression induces apoptosis and inhibits cell growth and migrationFrontiers in oncology · 2022Article
- Clinical values and potential pathways of miR-183-5p in gastric cancer: a study based on integrational bioinformatics analysis.Journal of gastrointestinal oncology · 2021Article
- Identification of a novel circ_0018289/miR-183-5p/TMED5 regulatory network in cervical cancer development.World journal of surgical oncology · 2021Article
- Programmed cell death, redox imbalance, and cancer therapeutics.Apoptosis : an international journal on programmed cell death · 2021Review
- Traditional Chinese Medicine and Colorectal Cancer: Implications for Drug Discovery.Frontiers in pharmacology · 2021Review
- Shikonin inhibits migration and invasion of triple-negative breast cancer cells by suppressing epithelial-mesenchymal transition via miR-17-5p/PTEN/Akt pathway.Journal of Cancer · 2021Article
- Shikonin suppresses the epithelial-to-mesenchymal transition by downregulating NHE1 in bladder cancer cells.Journal of Cancer · 2021Article
- Anti-Tumor Mechanisms Associated With Regulation of Non-Coding RNA by Active Ingredients of Chinese Medicine: A Review.Frontiers in oncology · 2020Review
- MiR-183-5p promotes renal cell carcinoma metastasis by targeting TET1.International journal of immunopathology and pharmacologyArticle
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundShikonin, the main ingredient of
methodsMTT, wound-healing, transwell assays and flow cytometry experiments were used to measure cell growth, migration, invasion, and cell cycle analysis. Western blot was used to examine protein levels of Snail, Vimentin and E-cadherin. The expression level of miR-183-5p was measured via qRT-PCR. The E-cadherin promoter activity was detected via Secrete-PairTM Dual Luminescence Assay Kit. The transient transfection experiments were used for silencing of E-cadherin and overexpression of Snail genes. Tumor xenograft and bioluminescent imaging experiments were carried out to confirm the in vitro findings.
resultsWe showed that shikonin inhibited cell viability, migration and invasion, and induced cell cycle arrest in a dose-dependent manner in cervical cancer Hela and C33a cells. Mechanistically, we found that shikonin increased miR-183-5p expression and inhibited expression of transcription factor Snail protein. The mimics of miR-183-5p reduced, while the inhibitors of miR-183-5p reversed shikonin-inhibited Snail protein expression. In addition, shikonin decreased Vimentin, increased E-cadherin protein expressions and E-cadherin promoter activity, the latter was reversed in cells transfected with exogenous Snail overexpression vectors. Moreover, silencing of E-cadherin significantly abolished shikonin-inhibited cervical cancer cell growth. Similar findings were also observed in vivo using one xenograft mouse model.
conclusionOur results show that shikonin inhibits EMT through inhibition of Snail and stimulation of miR-183-5p expressions, which resulted in induction of E-cadherin expression. Thus, blockade of EMT could be a novel mechanism underlying the anti-cervical cancer effects of shikonin.
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