PMID- 34554318
OWN - NLM
STAT- MEDLINE
DCOM- 20220802
LR  - 20220803
IS  - 1591-9528 (Electronic)
IS  - 1591-8890 (Print)
IS  - 1591-8890 (Linking)
VI  - 22
IP  - 3
DP  - 2022 Aug
TI  - PEAK1 promotes invasion and metastasis and confers drug resistance in breast 
      cancer.
PG  - 393-402
LID - 10.1007/s10238-021-00761-5 [doi]
AB  - Pseudopodium-enriched atypical kinase 1 (PEAK1) has been reported to be 
      upregulated in human malignancies and is correlated with a poor prognosis. 
      Enhanced PEAK1 expression facilitates tumor cell survival, invasion, metastasis 
      and chemoresistance. However, the role of PEAK1 in breast cancer is unclear. We 
      investigated PEAK1 expression in breast cancer and analyzed the relationship with 
      clinicopathological status and chemotherapy resistance. We also investigated the 
      role of PEAK1 in breast cancer cells in vitro and in vivo. Immunohistochemistry 
      for PEAK1 was performed in 112 surgically resected breast cancer tissues. The 
      association between clinicopathological status, chemotherapy resistance and PEAK1 
      expression was determined. The effect of PEAK1 overexpression or downregulation 
      on proliferation, colony formation, invasion, migration, metastasis and 
      doxorubicin sensitivity in MCF-7 cells in vitro and in vivo was studied. PEAK1 
      was overexpressed in breast cancer tissues. High PEAK1 expression was correlated 
      with tumor size, high tumor grade, tumor stage, lymph node metastasis, 
      recurrence, Ki-67 expression, Her-2 expression and chemotherapy resistance. 
      Inhibiting PEAK1 decreased cell growth, invasion, metastasis and reversed 
      chemoresistance to doxorubicin in breast cancer cells both in vitro and in vivo. 
      High PEAK1 expression was associated with the invasion, metastasis and 
      chemoresistance of breast cancers. Furthermore, targeting PEAK1 inhibited cell 
      growth and metastasis and reversed chemoresistance in breast cancer cells. 
      Targeting PEAK1 could be an effective treatment strategy for breast cancer.
CI  - (c) 2021. The Author(s).
FAU - Wang, Xingang
AU  - Wang X
AD  - Department of Breast Surgery, The Affiliated Hospital of Qingdao University, 
      Qingdao, 266003, Shandong, China.
FAU - Zheng, Yan
AU  - Zheng Y
AD  - Department of Operating Room, The Affiliated Hospital of Qingdao University, 
      Qingdao, 266003, Shandong, China.
FAU - Wang, Yu
AU  - Wang Y
AUID- ORCID: 0000-0003-1379-7736
AD  - Department of Breast Surgery, The Affiliated Hospital of Qingdao University, 
      Qingdao, 266003, Shandong, China. qyfywang@163.com.
LA  - eng
PT  - Journal Article
DEP - 20210923
PL  - Italy
TA  - Clin Exp Med
JT  - Clinical and experimental medicine
JID - 100973405
RN  - 80168379AG (Doxorubicin)
RN  - EC 2.7.10.1 (PEAK1 protein, human)
RN  - EC 2.7.10.1 (Protein-Tyrosine Kinases)
SB  - IM
MH  - *Breast Neoplasms/drug therapy/pathology
MH  - Cell Line, Tumor
MH  - Cell Movement
MH  - Cell Proliferation
MH  - Doxorubicin/pharmacology
MH  - *Drug Resistance, Neoplasm
MH  - Female
MH  - Gene Expression Regulation, Neoplastic
MH  - Humans
MH  - MCF-7 Cells
MH  - Neoplasm Metastasis
MH  - *Protein-Tyrosine Kinases/metabolism
MH  - Pseudopodia/metabolism
MH  - Signal Transduction
PMC - PMC9338157
OTO - NOTNLM
OT  - Breast cancer
OT  - Chemotherapy resistance
OT  - Metastasis
OT  - Pseudopodium-enriched atypical kinase 1
COIS- The authors declare that they have no competing interests.
EDAT- 2021/09/24 06:00
MHDA- 2022/08/03 06:00
PMCR- 2021/09/23
CRDT- 2021/09/23 12:26
PHST- 2021/05/21 00:00 [received]
PHST- 2021/09/03 00:00 [accepted]
PHST- 2021/09/24 06:00 [pubmed]
PHST- 2022/08/03 06:00 [medline]
PHST- 2021/09/23 12:26 [entrez]
PHST- 2021/09/23 00:00 [pmc-release]
AID - 10.1007/s10238-021-00761-5 [pii]
AID - 761 [pii]
AID - 10.1007/s10238-021-00761-5 [doi]
PST - ppublish
SO  - Clin Exp Med. 2022 Aug;22(3):393-402. doi: 10.1007/s10238-021-00761-5. Epub 2021 
      Sep 23.