ArticleMolecular medicine reports2021
RHBDD1 promotes proliferation, migration, invasion and EMT in renal cell carcinoma via the EGFR/AKT signaling pathway.
Article in Molecular medicine reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 12 citations in OpenAlex.
- RHBDD1 induces cell cycle arrest in TP53-mutant NSCLC cells by promoting endoplasmic reticulum-associated degradation of p53 and DNA-PKcs.European journal of medical research · 2025Article
- Targeting EGFR/IGF-IR Functional Crosstalk in 2D and 3D Triple-Negative Breast Cancer Models to Evaluate Tumor Progression.International journal of molecular sciences · 2025Article
- RHBDD1 Promotes the Growth and Stemness Characteristics of Gastric Cancer Cells by Activating Wnt/β-catenin Signaling Pathway.Current stem cell research & therapy · 2024Article
- Smoking enhanced the expression of c-kit in chromophobe renal cell carcinoma.Tobacco induced diseases · 2023Article
- A cuproptosis-related lncRNA signature identified prognosis and tumour immune microenvironment in kidney renal clear cell carcinoma.Frontiers in molecular biosciences · 2022Article
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
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Abstract
Renal cell carcinoma (RCC) is a common malignant tumor of the urinary system with a poor prognosis and high mortality rate. The increasing incidence of RCC poses a serious threat to human health. It is well‑documented that rhomboid domain‑containing protein 1 (RHBDD1) plays a vital role in cancer progression. The present study was designed to identify the biological functions of RHBDD1 in RCC and investigate the underlying regulatory mechanism, aiming to explore the novel molecular therapeutic targets for RCC. The protein and mRNA expression levels of RHBDD1 in normal renal tubule epithelium and human RCC cell lines were analyzed using western blotting and reverse transcription‑quantitative PCR. Cell proliferation was determined using Cell Counting Kit‑8 assays. Wound healing and Transwell assays were performed to determine cell migration and invasion, respectively. In addition, key proteins related to migration, invasion and epithelial‑mesenchymal transition (EMT), such as matrix metalloproteinase (MMP)2, MMP9, MMP13, E‑cadherin, N‑cadherin, vimentin and Slug, were analyzed using western blotting. In addition, the EGFR/AKT signaling pathway was further studied using western blotting to determine the potential molecular mechanism. The results of the present study revealed that RHBDD1 expression levels were significantly upregulated in RCC cell lines. The knockdown of RHBDD1 inhibited cell proliferation, migration, invasion and EMT, while the overexpression of RHBDD1 promoted cell proliferation, migration, invasion and EMT in RCC. In addition, the knockdown of RHBDD1 suppressed the activation of the EGFR/AKT signaling pathway, while the overexpression of RHBDD1 activated the EGFR/AKT signaling pathway. Moreover, these stimulatory effects of RHBDD1 overexpression on RCC progression and the EGFR/AKT signaling pathway were partly reversed by gefitinib, an EGFR inhibitor. In conclusion, the findings of the present study suggested that RHBDD1 may be a crucial regulator of RCC by modulating the EGFR/AKT signaling pathway. The present study may provide a theoretical basis and potential targets for RCC treatment.
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