ArticlePathology oncology research : POR2021
Tuftelin 1 (TUFT1) Promotes the Proliferation and Migration of Renal Cell Carcinoma
Article in Pathology oncology research : POR, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 26 citations in OpenAlex.
- TUFT1 stabilizes TGF-β receptor II protein and facilitates activation of hepatic stellate cells into metastasis-promoting myofibroblasts.Cell death and differentiation · 2026Article
- TUFT1 regulates cancer progression by suppressing centrosome amplification and mitotic spindle multipolarity.Cell death & disease · 2025Article
- TUFT1 Modulates Cell Proliferation, Migration, Invasion, Stemness and EGFR Signaling in Cervical Cancer through Interacting with and Targeting ATF1.Cell biochemistry and biophysics · 2025Article
- Non-SMC condensin I complex subunit H promotes cell proliferation and inhibits cell apoptosis of clear cell renal cell carcinoma by activating the PI3K/AKT pathway.Translational andrology and urology · 2025Article
- Investigating the role of exosomal long non-coding RNAs in drug resistance within female reproductive system cancers.Frontiers in cell and developmental biology · 2025Review
- Evaluation of Long Non-coding RNA (LncRNA) in the Pathogenesis of Chemotherapy Resistance in Cervical Cancer: Diagnostic and Prognostic Approach.Molecular biotechnology · 2024Review
- Tuftelin1 drives experimental pulmonary fibrosis progression by facilitating stress fiber assembly.Respiratory research · 2023Article
- TAGLN2 Promotes the Proliferation, Migration, Invasion, and EMT of Clear Cell Renal Cell Carcinoma Through the PI3K/Akt Signaling Pathway.Biochemical genetics · 2023Article
- microRNA-128-3p inhibits proliferation and accelerates apoptosis of gastric cancer cells via inhibition of TUFT1.World journal of surgical oncology · 2023Article
- LINC00960 regulates cell proliferation and glycolysis in pancreatic cancer through the miR-326-3p/TUFT1/AKT-mTOR axis.The Kaohsiung journal of medical sciences · 2022Article
- Small Extracellular Vesicles and Their Involvement in Cancer Resistance: An Up-to-Date Review.Cells · 2022Review
- Morphological and Molecular Responses ofInternational journal of molecular sciences · 2022Article
- m7G regulator-mediated molecular subtypes and tumor microenvironment in kidney renal clear cell carcinoma.Frontiers in pharmacology · 2022Article
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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
Tuftelin 1 (TUFT1), a protein functioning distinctively in different tissues, is reported to be elevated in several types of cancers and the elevation of TUFT1 is correlated with unfavorable clinicopathologic characteristics and poor survival. However, the involvement of TUFT1 in renal cell carcinoma (RCC) remains unknown. In the current study, we investigated the role of TUFT1 in RCC and potential underlying mechanisms. RT-PCR and Western blot analysis showed that both the mRNA and protein levels of TUFT1 were increased in primary RCC tissue and RCC cell lines. TUFT1 overexpression in RCC cells resulted in enhanced cell proliferation and migration while knockdown of TUFT1 by contrast decreased the growth and migration of the RCC cells, indicating TUFT1 expression is involved in RCC cell growth and migration. The involvement of TUFT1 in the epithelial-mesenchymal transition (EMT) of RCC cells was also determined by measuring the expression of EMT-related markers. Our data showed that TUFT1 overexpression promoted RCC cell EMT progression while knockdown of TUFT1 suppressed such process. Further signaling pathway inhibition assay revealed that TUFT1-induced RCC cell growth, migration and EMT was significantly suppressed by PI3K inhibitor, but not JNK or MEK inhibitors. In addition, TUFT1 overexpression enhanced the AKT phosphorylation, a key member of the PI3K signaling pathway, while PI3K inhibitor suppressed such process. Taken together, our study showed that TUFT1 expression was elevated in RCC and such elevation promoted the proliferation, migration and EMT of RCC cells
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