Related Experiment Video
Updated: May 31, 2025

In vitro Organoid Culture of Primary Mouse Colon Tumors
Published on: May 17, 2013
CKAP2L Plays a Pivotal Role in Colorectal Cancer Progression via the Dual Regulation of Cell Cycle and
Qingbin Luo1, Bohui Zhu2, Cuilan Wang1
1Department of Radiation Oncology, Anhui Zhongke Genjiu Hospital, 230051 Hefei, Anhui, China.
Background:
Cytoskeleton-associated protein 2 like (CKAP2L) has been demonstrated to mediate the cell cycle in cancer cells. However, it is unknown whether CKAP2L impacts colorectal cancer (CRC). The purpose of this study was to investigate the role of CKAP2L in CRC.
Methods:
CKAP2L and regulatory factor X 5 (RFX5) expression profiles in colon adenocarcinoma (COAD) and rectal adenocarcinoma (READ) were analyzed in UALCAN. Human colorectal adenocarcinoma epithelial cells, DLD1, were transfected with small interfering RNA targeting RFX5 and CKAP2L-overexpressing vectors (OE-CKAP2L). The interaction between CKAP2L and RFX5 was identified by dual-luciferase assay and chromatin immunoprecipitation. Epithelial-mesenchymal transition (EMT)- and protein kinase B/mammalian target of the rapamycin (AKT/mTOR) pathway-associated proteins were evaluated by western blotting.
Results:
RFX5 and CKAP2L expression was increased in CRC based on the UALCAN database. RFX5 downregulation inhibited proliferation, migration, invasion, and EMT while promoting G1/S phase arrest (p < 0.01). RFX5 knockdown downregulated CKAP2L expression and mediated the inactivation of the AKT/mTOR pathway (p < 0.001). RFX5 acted as an upstream transcription factor of CKAP2L. CKAP2L overexpression attenuated the restriction of RFX5 downregulation on CRC cell malignant phenotypes (p < 0.01).
Conclusion:
CKAP2L transcriptionally activated by RFX5 accelerates CRC proliferation and metastasis by promoting the cell cycle and EMT. This study provides potential molecular targets for treating CRC.
Related Concept Videos
Tumor Progression
Colon cancer is one of the best-documented examples of tumor progression. Early mutation in the APC gene in colon cells causes a small growth on the colon wall called a polyp. With time, this polyp grows into a benign, pre-cancerous tumor. Further...
M-Cdk Drives Transition Into Mitosis
Cyclin-dependent kinases, or Cdks, work in concert with cyclins to control cell cycle transitions. M-Cdk, a complex of Cdk1 bound to M cyclin, is a well-known example of this coordinated control that drives the transition from the G2 to the M phase.
M cyclin...
Inhibition of Cdk Activity
Positive Regulator Molecules
MAPK Signaling Cascades
mTOR Signaling and Cancer Progression
The mTOR pathway or the...

