ArticleExperimental and therapeutic medicine2017
Silencing of TCTN1 inhibits proliferation, induces cell cycle arrest and apoptosis in human thyroid cancer.
Article in Experimental and therapeutic medicine, 2017. 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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Who cites it
11 citing papers in PubMed, 12 citations in OpenAlex.
- Article
- Circular RNA circCHSY1 silencing inhibits the malignant progression of esophageal squamous cell carcinoma.Discover oncology · 2024Article
- Molecular mechanisms of microRNA-216a during tumor progression.Cancer cell international · 2023Review
- Life-Saver or Undertaker: The Relationship between Primary Cilia and Cell Death in Vertebrate Embryonic Development.Journal of developmental biology · 2022Review
- Simvastatin Attenuated Tumor Growth in Different Pancreatic Tumor Animal Models.Pharmaceuticals (Basel, Switzerland) · 2022Article
- Function and transcriptional regulation of TCTN1 in oral squamous cell carcinoma.Oncology reports · 2022Article
- Downregulated LRRK2 gene expression inhibits proliferation and migration while promoting the apoptosis of thyroid cancer cells by inhibiting activation of the JNK signaling pathway.International journal of oncology · 2019Article
- The treatment role ofBioscience reports · 2019Article
- MiR-216a-5p targets TCTN1 to inhibit cell proliferation and induce apoptosis in esophageal squamous cell carcinoma.Cellular & molecular biology letters · 2019Article
- Norcantharidin inhibits viability and induces cell cycle arrest and apoptosis in osteosarcoma.Oncology letters · 2019Article
- Dual Roles of Ascidian Chondromodulin-1: Promoting Cell Proliferation Whilst Suppressing the Growth of Tumor Cells.Marine drugs · 2018Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tectonic family member 1 (TCTN1) is one of the tectonic family members, and a regulator of the hedgehog signaling pathway, which has been studied in various cancer types, including prostate and pancreatic cancer. However, its function in thyroid cancer has not been well documented. Therefore, the present study investigated the function of TCTN1 in thyroid cancer using a loss-of-function assay. Lentivirus-mediated RNA interference was applied to downregulate TCTN1 in the thyroid cancer cell lines, CAL62 and 8305C. A series of functional properties, including cell viability, colony formation, cell cycle and apoptosis were determined using MTT, colony formation assay and flow cytometry analyses, respectively. The results demonstrated that lentivirus-medicated RNAi could specifically suppress the expression of TCTN1 at the mRNA and protein levels in CAL62, and 8305C cells. Knockdown of TCTN1 inhibited cell growth and proliferation via inducing S phase arrest, and apoptosis. Mechanistically, the S phase arrest was accompanied by the upregulation of cyclin dependent kinase 2, cyclin A2 and downregulation of cyclin B1. Knockdown of TCTN1 induced apoptosis through increasing the expression of Bcl2-associated agonist of cell death, cleaved caspase-3 and poly(ADP-ribose)polymerase, and decreasing apoptosis regulator Bcl-2 expression. The current study highlights the essential role of TCTN1 in promoting thyroid cancer cell proliferation, and its knockdown may serve as a potential therapeutic treatment for thyroid cancer.
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