DKK1 as a chemoresistant protein modulates oxaliplatin responses in colorectal cancer

Oxaliplatin is effective against colorectal cancer (CRC), but resistance hampers treatment. We found upregulated Dickkopf-1 (DKK1, a secreted protein) in oxaliplatin-resistant (OR) CRC cell lines and DKK1 levels increased by more than 2-fold in approximately 50% of oxaliplatin-resistant CRC tumors. DKK1 activates AKT via cytoskeleton-associated protein 4 (CKAP4, a DKK1 receptor), modulating oxaliplatin responses in vitro and in vivo. The leucine zipper (LZ) domain of CKAP4 and cysteine-rich domain 1 (CRD1) of secreted DKK1 are crucial for their interaction and AKT signaling. By utilizing the LZ protein, we disrupted DKK1 signaling, enhancing oxaliplatin sensitivity in OR CRC cells and xenograft tumors. This suggests that DKK1 as a chemoresistant factor in CRC via AKT activation. Targeting DKK1 with the LZ protein offers a promising therapeutic strategy for oxaliplatin-resistant CRC with high DKK1 levels. This study sheds light on oxaliplatin resistance mechanisms and proposes an innovative intervention for managing this challenge.

Authors

Institutions

Publication Details

Journal
Oncogenesis
Published
2024-09-27
DOI
https://doi.org/10.1038/s41389-024-00537-y
Citations
11
Primary Topic
Colorectal Cancer Treatments and Studies
Type
article
Field-Weighted Citation Impact
3.11

Funders

Controls
|||
ALL TIME
JAN
FEB
MAR
APR
MAY
JUN
JUL
AUG
SEP
OCT
article

DKK1 as a chemoresistant protein modulates oxaliplatin responses in colorectal cancer

Nai-Jung Chiang, Tingwei Li, Che‐Hung Shen, Chun-Chun Li et al.
11 citations
Oncogenesis
Colorectal Cancer Treatments and Studies
3.11
article

DKK1 as a chemoresistant protein modulates oxaliplatin responses in colorectal cancer

Nai-Jung Chiang, Tingwei Li, Che‐Hung Shen, Chun-Chun Li, Chi–Che Hsieh, You-Lin Wei, Shang-Hung Chen
article en
11 citations

Abstract

Oxaliplatin is effective against colorectal cancer (CRC), but resistance hampers treatment. We found upregulated Dickkopf-1 (DKK1, a secreted protein) in oxaliplatin-resistant (OR) CRC cell lines and DKK1 levels increased by more than 2-fold in approximately 50% of oxaliplatin-resistant CRC tumors. DKK1 activates AKT via cytoskeleton-associated protein 4 (CKAP4, a DKK1 receptor), modulating oxaliplatin responses in vitro and in vivo. The leucine zipper (LZ) domain of CKAP4 and cysteine-rich domain 1 (CRD1) of secreted DKK1 are crucial for their interaction and AKT signaling. By utilizing the LZ protein, we disrupted DKK1 signaling, enhancing oxaliplatin sensitivity in OR CRC cells and xenograft tumors. This suggests that DKK1 as a chemoresistant factor in CRC via AKT activation. Targeting DKK1 with the LZ protein offers a promising therapeutic strategy for oxaliplatin-resistant CRC with high DKK1 levels. This study sheds light on oxaliplatin resistance mechanisms and proposes an innovative intervention for managing this challenge.

OncogenesisVol. 13(1)
National Yang Ming Chiao Tung University (TW), Kaohsiung Medical University (TW), National Chung Hsing University (TW), National Health Research Institutes (TW), Taipei Veterans General Hospital (TW), National Cheng Kung University Hospital (TW), Taipei Medical University (TW), National Cheng Kung University (TW)
Ministry of Science and Technology, Taiwan, National Health Research Institutes, National Cheng Kung University Hospital, National Cheng Kung University, Taipei Veterans General Hospital, National Science and Technology Council
Good health and well-being
Openalex Percentile: Top 7%
Colorectal Cancer Treatments and Studies
3.11
AI Navigator

Ask Laika to Summarize, Analyze, and Connect papers live on the map.

Summarize Papers & Methodologies

Extract key findings, datasets, and comparative methods across publications.

Benchmark Rankings & Visual Analytics

Rank top research institutions, authors, funders, topics, and journals by Field-Weighted Citation Impact (FWCI) and paper volume with instant charts.

Connect Distant Disciplines

Bridge topological clusters on the map to find hidden collaborative intersections.