Related Experiment Video
Updated: Mar 3, 2026

Studying TGF-β Signaling and TGF-β-induced Epithelial-to-mesenchymal Transition in Breast Cancer and Normal Cells
Published on: October 27, 2020
RCCD1 depletion attenuates TGF-β-induced EMT and cell migration by stabilizing cytoskeletal microtubules in NSCLC
Junyu Wu1, Zhimin He2, Xiao-Mei Yang3
1Research Centre for Translational Medicine at East Hospital, School of Life Sciences and Technology, Tongji University, Shanghai 200092/200120, China; Department of Basic Medical Sciences, School of Medicine, Tsinghua University, Beijing 100084, China.
Abstract:
Lung cancer is one of the most lethal cancers due to its highly metastatic spreading. The motility of lung cancer cells is regulated by paracrine factors, such as TGF-β, in the tumor microenvironment through the induction of epithelial-to-mesenchymal transition (EMT). The stability of microtubules is reported to be associated with the EMT process and the migration of cancer cells. Here, we observed that RCC1 domain-containing protein 1 (RCCD1) is highly expressed in non-small cell lung cancer (NSCLC) patients with poor prognosis, and RCCD1 is much higher expressed in tumor tissues compared with adjacent normal tissues. Depletion of RCCD1 using siRNAs significantly inhibits the migration of lung cancer cells. Subsequent studies reveal that the loss of RCCD1 results in upregulation of acetylated α-tubulin levels and stabilizes cytoskeletal microtubules. Mechanistically, we observed that RCCD1 modulates the stability of microtubules through interacting with JMJD5. Furthermore, RCCD1 depletion significantly attenuates the TGF-β-induced EMT process, as assessed by altered expression of epithelial and mesenchymal markers (Occludin, Vimentin and Snail), and inhibits TGF-β-induced cell migration. Collectively, these findings support RCCD1 as a novel regulator of TGF-β-induced EMT in NSCLC.
Insights
RCCD1 protein promotes lung cancer cell migration by regulating microtubule stability and epithelial-to-mesenchymal transition (EMT). Inhibiting RCCD1 may offer a new strategy for treating non-small cell lung cancer (NSCLC).
Area of Science:
- Oncology
- Cell Biology
- Molecular Medicine
Background:
- Lung cancer exhibits high metastatic potential, driven by cell motility regulated by factors like TGF-β.
- Epithelial-to-mesenchymal transition (EMT) and microtubule stability are crucial for cancer cell migration.
- The role of RCCD1 in non-small cell lung cancer (NSCLC) metastasis requires further elucidation.
Purpose of the Study:
- To investigate the role of RCCD1 in NSCLC progression and metastasis.
- To elucidate the molecular mechanisms by which RCCD1 influences cancer cell motility and EMT.
- To assess the therapeutic potential of targeting RCCD1 in NSCLC.
Main Methods:
- Analysis of RCCD1 expression in NSCLC patient tissues and correlation with prognosis.
- siRNA-mediated depletion of RCCD1 to assess its impact on lung cancer cell migration.
- Investigation of RCCD1's interaction with JMJD5 and its effect on microtubule acetylation and stability.
- Assessment of TGF-β-induced EMT markers and cell migration following RCCD1 depletion.
Main Results:
- RCCD1 is highly expressed in NSCLC tumors and associated with poor prognosis.
- RCCD1 depletion significantly inhibits lung cancer cell migration.
- RCCD1 modulates microtubule stability via interaction with JMJD5, leading to increased acetylated α-tubulin.
- RCCD1 depletion attenuates TGF-β-induced EMT and cell migration.
Conclusions:
- RCCD1 acts as a novel regulator of TGF-β-induced EMT in NSCLC.
- RCCD1 promotes lung cancer cell migration by stabilizing microtubules.
- Targeting RCCD1 presents a potential therapeutic strategy for NSCLC.
Related Concept Videos
Cell Polarization by Rho Proteins
Small GTPases - Ras and Rho
Three regulatory proteins control their activity:
TGF - β Signaling Pathway
Cell Motility through Blebbing
Blebbing Through the Matrix
In multicellular...
Cadherins in Tissue Organization
Cell Sorting During Development
Cell sorting plays an...
The Retinoblastoma Gene
The first-ever tumor suppressor gene called Rb was identified in retinoblastoma - a rare eye tumor in children. In inherited forms of the disease, a child inherits one defective copy of the Rb gene, which predisposes them to retinoblastoma. However,...

