Hoe Peng Liew
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Research Interests
Hoe Peng Liew has a total of 13 co-authors. Here are the top co-authors by number of shared publications:
- Angela Takano
Department of Pathology, Histopathology Section, Singapore General Hospital, Singapore 169856, Singapore
1 shared publication - Axel Ullrich
Department of Molecular Biology, Max-Planck-Institute of Biochemistry, Martinsried, Germany
1 shared publication - Benjamin Haaland
Duke-NUS Graduate Medical School, Singapore 169857, Singapore
1 shared publication - Boon Tin Chua
INM-SOG, Institute of Molecular and Cell Biology, Agency of Science Technology and Research, Singapore, Singapore
1 shared publication - Daniel Shao Weng Tan
Division of Medical Oncology, National Cancer Centre Singapore, Singapore, Singapore
1 shared publication - Eng-Huat Tan
Department of Medical Oncology, National Cancer Centre, Singapore
1 shared publication
Latest Publications
- Open Access
- 24 January 2014
- Published by Springer Nature in Molecular Cancer
- Vol. 13 (1) , 13
Bosutinib inhibits migration and invasion via ack1 in kras mutant non-small cell lung cancer
The advent of effective targeted therapeutics has led to increasing emphasis on precise biomarkers for accurate patient stratification. Here, we describe the role of ACK1, a non-receptor tyrosine kinase in abrogating migration and invasion in KRAS mutant lung adenocarcinoma. Bosutinib, which inhibits ACK1 at 2.7 nM IC50, was found to inhibit cell migration and invasion but not viability in a panel of non-small cell lung cancer (NSCLC) cell lines. Knockdown of ACK1 abrogated bosutinib-induced inhibition of cell migration and invasion specifically in KRAS mutant cells. This finding was further confirmed in an in vivo zebrafish metastatic model. Tissue microarray data on 210 Singaporean lung adenocarcinomas indicate that cytoplasmic ACK1 was significantly over-expressed relative to paired adjacent non-tumor tissue. Interestingly, ACK1 expression in “normal” tissue adjacent to tumour, but not tumour, was independently associated with poor overall and relapse-free survival. In conclusion, inhibition of ACK1 with bosutinib attenuates migration and invasion in the context of KRAS mutant NSCLC and may fulfil a therapeutic niche through combinatorial treatment approaches.
- 24 January 2014
- Published by Springer Nature in Molecular Cancer
- Vol. 13 (1) , 13
Open AccessBosutinib inhibits migration and invasion via ack1 in kras mutant non-small cell lung cancer
The advent of effective targeted therapeutics has led to increasing emphasis on precise biomarkers for accurate patient stratification. Here, we describe the role of ACK1, a non-receptor tyrosine kinase in abrogating migration and invasion in KRAS mutant lung adenocarcinoma. Bosutinib, which inhibits ACK1 at 2.7 nM IC50, was found to inhibit cell migration and invasion but not viability in a panel of non-small cell lung cancer (NSCLC) cell lines. Knockdown of ACK1 abrogated bosutinib-induced inhibition of cell migration and invasion specifically in KRAS mutant cells. This finding was further confirmed in an in vivo zebrafish metastatic model. Tissue microarray data on 210 Singaporean lung adenocarcinomas indicate that cytoplasmic ACK1 was significantly over-expressed relative to paired adjacent non-tumor tissue. Interestingly, ACK1 expression in “normal” tissue adjacent to tumour, but not tumour, was independently associated with poor overall and relapse-free survival. In conclusion, inhibition of ACK1 with bosutinib attenuates migration and invasion in the context of KRAS mutant NSCLC and may fulfil a therapeutic niche through combinatorial treatment approaches.