PMID- 35986321
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20220826
IS  - 1475-2867 (Print)
IS  - 1475-2867 (Electronic)
IS  - 1475-2867 (Linking)
VI  - 22
IP  - 1
DP  - 2022 Aug 19
TI  - Anti-cancer therapeutic strategies based on HGF/MET, EpCAM, and tumor-stromal 
      cross talk.
PG  - 259
LID - 10.1186/s12935-022-02658-z [doi]
LID - 259
AB  - As an intelligent disease, tumors apply several pathways to evade the immune 
      system. It can use alternative routes to bypass intracellular signaling pathways, 
      such as nuclear factor-kappaB (NF-kappaB), Wnt, and mitogen-activated protein 
      (MAP)/phosphoinositide 3-kinase (PI3K)/mammalian target of rapamycin (mTOR). 
      Therefore, these mechanisms lead to therapeutic resistance in cancer. Also, these 
      pathways play important roles in the proliferation, survival, migration, and 
      invasion of cells. In most cancers, these signaling pathways are overactivated, 
      caused by mutation, overexpression, etc. Since numerous molecules share these 
      signaling pathways, the identification of key molecules is crucial to achieve 
      favorable consequences in cancer therapy. One of the key molecules is the 
      mesenchymal-epithelial transition factor (MET; c-Met) and its ligand hepatocyte 
      growth factor (HGF). Another molecule is the epithelial cell adhesion molecule 
      (EpCAM), which its binding is hemophilic. Although both of them are involved in 
      many physiologic processes (especially in embryonic stages), in some cancers, 
      they are overexpressed on epithelial cells. Since they share intracellular 
      pathways, targeting them simultaneously may inhibit substitute pathways that 
      tumor uses to evade the immune system and resistant to therapeutic agents.
CI  - (c) 2022. The Author(s).
FAU - Barzaman, Khadijeh
AU  - Barzaman K
AD  - Recombinant Proteins Department, Breast Cancer Research Center, Motamed Cancer 
      Institute, ACECR, Tehran, Iran.
AD  - Department of Immunology, School of Medicine, Iran University of Medical 
      Sciences, Tehran, Iran.
FAU - Vafaei, Rana
AU  - Vafaei R
AD  - Recombinant Proteins Department, Breast Cancer Research Center, Motamed Cancer 
      Institute, ACECR, Tehran, Iran.
AD  - Department of Clinical Pathology, Faculty of Veterinary Medicine, University of 
      Tehran, Tehran, Iran.
FAU - Samadi, Mitra
AU  - Samadi M
AD  - Recombinant Proteins Department, Breast Cancer Research Center, Motamed Cancer 
      Institute, ACECR, Tehran, Iran.
FAU - Kazemi, Mohammad Hossein
AU  - Kazemi MH
AD  - Recombinant Proteins Department, Breast Cancer Research Center, Motamed Cancer 
      Institute, ACECR, Tehran, Iran.
AD  - ATMP Department, Breast Cancer Research Center, Motamed Cancer Institute, ACECR, 
      Tehran, Iran.
FAU - Hosseinzadeh, Aysooda
AU  - Hosseinzadeh A
AD  - Recombinant Proteins Department, Breast Cancer Research Center, Motamed Cancer 
      Institute, ACECR, Tehran, Iran.
FAU - Merikhian, Parnaz
AU  - Merikhian P
AD  - Recombinant Proteins Department, Breast Cancer Research Center, Motamed Cancer 
      Institute, ACECR, Tehran, Iran.
FAU - Moradi-Kalbolandi, Shima
AU  - Moradi-Kalbolandi S
AD  - Recombinant Proteins Department, Breast Cancer Research Center, Motamed Cancer 
      Institute, ACECR, Tehran, Iran.
FAU - Eisavand, Mohammad Reza
AU  - Eisavand MR
AD  - Recombinant Proteins Department, Breast Cancer Research Center, Motamed Cancer 
      Institute, ACECR, Tehran, Iran.
FAU - Dinvari, Houra
AU  - Dinvari H
AD  - Recombinant Proteins Department, Breast Cancer Research Center, Motamed Cancer 
      Institute, ACECR, Tehran, Iran.
FAU - Farahmand, Leila
AU  - Farahmand L
AUID- ORCID: 0000-0003-4548-3424
AD  - Recombinant Proteins Department, Breast Cancer Research Center, Motamed Cancer 
      Institute, ACECR, Tehran, Iran. laylafarahmand@gmail.com.
LA  - eng
PT  - Journal Article
PT  - Review
DEP - 20220819
PL  - England
TA  - Cancer Cell Int
JT  - Cancer cell international
JID - 101139795
PMC - PMC9389806
OTO - NOTNLM
OT  - EpCAM
OT  - HGF/MET
OT  - MAP/PI3K/mTOR
OT  - NF-kappaB
OT  - Wnt
COIS- The authors declare no competing interests.
EDAT- 2022/08/20 06:00
MHDA- 2022/08/20 06:01
PMCR- 2022/08/19
CRDT- 2022/08/19 23:37
PHST- 2021/09/08 00:00 [received]
PHST- 2022/07/19 00:00 [accepted]
PHST- 2022/08/19 23:37 [entrez]
PHST- 2022/08/20 06:00 [pubmed]
PHST- 2022/08/20 06:01 [medline]
PHST- 2022/08/19 00:00 [pmc-release]
AID - 10.1186/s12935-022-02658-z [pii]
AID - 2658 [pii]
AID - 10.1186/s12935-022-02658-z [doi]
PST - epublish
SO  - Cancer Cell Int. 2022 Aug 19;22(1):259. doi: 10.1186/s12935-022-02658-z.