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The effects and mechanisms of SLC34A2 on maintaining stem cell-like phenotypes in CD147(+) breast cancer stem cells.

Abstract The cancer stem cell (CSC) hypothesis has gained significant recognition in describing tumorigenesis. Identification of the factors critical to development of breast cancer stem cells (BCSCs) may provide insight into the improvement of effective therapies against breast cancer. In this study, we aim to investigate the biological function of SLC34A2 in affecting the stem cell-like phenotypes in BCSCs and its underlying mechanisms. We demonstrated that CD147(+) cells from breast cancer tissue samples and cell lines possessed BCSC-like features, including the ability of self-renewal in vitro, differentiation, and tumorigenic potential in vivo. Flow cytometry analysis showed the presence of a variable fraction of CD147(+) cells in 9 of 10 tumor samples. Significantly, SLC34A2 expression in CD147(+) BCSCs was enhanced compared with that in differentiated adherent progeny of CD147(+) BCSCs and adherently cultured cell line cells. In breast cancer patient cohorts, SLC34A2 expression was found increased in 9 of 10 tumor samples. By using lentiviral-based approach, si-SLC34A2-transduced CD147(+) BCSCs showed decreased ability of sphere formation, cell viability in vitro, and tumorigenicity in vivo, which suggested the essential role of SLC34A2 in CD147(+) BCSCs. Furthermore, PI3K/AKT pathway and SOX2 were found necessary to maintain the stemness of CD147(+) BCSCs by using LY294002 or lentiviral-si-SOX2. Finally, we indicated that SLC34A2 could regulate SOX2 to maintain the stem cell-like features in CD147(+) BCSCs through PI3K/AKT pathway. Therefore, our report identifies a novel role of SLC34A2 in BCSCs' state regulation and establishes a rationale for targeting the SLC34A2/PI3K/AKT/SOX2 signaling pathway for breast cancer therapy.
PMID
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Authors

Mayor MeshTerms
Keywords

Breast cancer stem cells

CD147

PI3K/AKT pathway

SLC34A2

SOX2

stem cell-like phenotypes

Journal Title tumour biology : the journal of the international society for oncodevelopmental biology and medicine
Publication Year Start




PMID- 28381172
OWN - NLM
STAT- MEDLINE
DA  - 20170406
DCOM- 20170418
LR  - 20170418
IS  - 1423-0380 (Electronic)
IS  - 1010-4283 (Linking)
VI  - 39
IP  - 4
DP  - 2017 Apr
TI  - The effects and mechanisms of SLC34A2 on maintaining stem cell-like phenotypes in
      CD147+ breast cancer stem cells.
PG  - 1010428317695927
LID - 10.1177/1010428317695927 [doi]
AB  - The cancer stem cell (CSC) hypothesis has gained significant recognition in
      describing tumorigenesis. Identification of the factors critical to development
      of breast cancer stem cells (BCSCs) may provide insight into the improvement of
      effective therapies against breast cancer. In this study, we aim to investigate
      the biological function of SLC34A2 in affecting the stem cell-like phenotypes in 
      BCSCs and its underlying mechanisms. We demonstrated that CD147+ cells from
      breast cancer tissue samples and cell lines possessed BCSC-like features,
      including the ability of self-renewal in vitro, differentiation, and tumorigenic 
      potential in vivo. Flow cytometry analysis showed the presence of a variable
      fraction of CD147+ cells in 9 of 10 tumor samples. Significantly, SLC34A2
      expression in CD147+ BCSCs was enhanced compared with that in differentiated
      adherent progeny of CD147+ BCSCs and adherently cultured cell line cells. In
      breast cancer patient cohorts, SLC34A2 expression was found increased in 9 of 10 
      tumor samples. By using lentiviral-based approach, si-SLC34A2-transduced CD147+
      BCSCs showed decreased ability of sphere formation, cell viability in vitro, and 
      tumorigenicity in vivo, which suggested the essential role of SLC34A2 in CD147+
      BCSCs. Furthermore, PI3K/AKT pathway and SOX2 were found necessary to maintain
      the stemness of CD147+ BCSCs by using LY294002 or lentiviral-si-SOX2. Finally, we
      indicated that SLC34A2 could regulate SOX2 to maintain the stem cell-like
      features in CD147+ BCSCs through PI3K/AKT pathway. Therefore, our report
      identifies a novel role of SLC34A2 in BCSCs' state regulation and establishes a
      rationale for targeting the SLC34A2/PI3K/AKT/SOX2 signaling pathway for breast
      cancer therapy.
FAU - Lv, Yonggang
AU  - Lv Y
AD  - 1 Department of Vascular and Endocrine Surgery, Xijing Hospital, Fourth Military 
      Medical University, Xi'an, People's Republic of China.
FAU - Wang, Ting
AU  - Wang T
AD  - 1 Department of Vascular and Endocrine Surgery, Xijing Hospital, Fourth Military 
      Medical University, Xi'an, People's Republic of China.
FAU - Fan, Jing
AU  - Fan J
AD  - 1 Department of Vascular and Endocrine Surgery, Xijing Hospital, Fourth Military 
      Medical University, Xi'an, People's Republic of China.
FAU - Zhang, Zhenzhen
AU  - Zhang Z
AD  - 2 Biotecan Medical Diagnostics Co. Ltd., Zhangjiang Center for Translational
      Medicine, Shanghai, People's Republic of China.
FAU - Zhang, Juliang
AU  - Zhang J
AD  - 1 Department of Vascular and Endocrine Surgery, Xijing Hospital, Fourth Military 
      Medical University, Xi'an, People's Republic of China.
FAU - Xu, Cheng
AU  - Xu C
AD  - 2 Biotecan Medical Diagnostics Co. Ltd., Zhangjiang Center for Translational
      Medicine, Shanghai, People's Republic of China.
FAU - Li, Yongping
AU  - Li Y
AD  - 1 Department of Vascular and Endocrine Surgery, Xijing Hospital, Fourth Military 
      Medical University, Xi'an, People's Republic of China.
FAU - Zhao, Ge
AU  - Zhao G
AD  - 1 Department of Vascular and Endocrine Surgery, Xijing Hospital, Fourth Military 
      Medical University, Xi'an, People's Republic of China.
FAU - He, Chenyang
AU  - He C
AD  - 1 Department of Vascular and Endocrine Surgery, Xijing Hospital, Fourth Military 
      Medical University, Xi'an, People's Republic of China.
FAU - Meng, Huimin
AU  - Meng H
AD  - 1 Department of Vascular and Endocrine Surgery, Xijing Hospital, Fourth Military 
      Medical University, Xi'an, People's Republic of China.
FAU - Yang, Hua
AU  - Yang H
AD  - 1 Department of Vascular and Endocrine Surgery, Xijing Hospital, Fourth Military 
      Medical University, Xi'an, People's Republic of China.
FAU - Wang, Zhen
AU  - Wang Z
AD  - 3 Department of Orthopaedic, Xijing Hospital, Fourth Military Medical University,
      Xi'an, People's Republic of China.
FAU - Liu, Jiayun
AU  - Liu J
AD  - 4 Institute of Clinical Laboratory Medicine, Xijing Hospital, Fourth Military
      Medical University, Xi' an, People's Republic of China.
FAU - Chen, Jianghao
AU  - Chen J
AD  - 1 Department of Vascular and Endocrine Surgery, Xijing Hospital, Fourth Military 
      Medical University, Xi'an, People's Republic of China.
FAU - Wang, Ling
AU  - Wang L
AD  - 1 Department of Vascular and Endocrine Surgery, Xijing Hospital, Fourth Military 
      Medical University, Xi'an, People's Republic of China.
LA  - eng
PT  - Journal Article
PL  - United States
TA  - Tumour Biol
JT  - Tumour biology : the journal of the International Society for Oncodevelopmental
      Biology and Medicine
JID - 8409922
RN  - 0 (BSG protein, human)
RN  - 0 (SLC34A2 protein, human)
RN  - 0 (SOX2 protein, human)
RN  - 0 (SOXB1 Transcription Factors)
RN  - 0 (Sodium-Phosphate Cotransporter Proteins, Type IIb)
RN  - 136894-56-9 (Antigens, CD147)
RN  - EC 2.7.1.- (Phosphatidylinositol 3-Kinases)
RN  - EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
SB  - IM
MH  - Animals
MH  - Antigens, CD147/*analysis
MH  - Breast Neoplasms/*pathology
MH  - Female
MH  - Humans
MH  - Mice
MH  - Neoplastic Stem Cells/chemistry/*physiology
MH  - Phenotype
MH  - Phosphatidylinositol 3-Kinases/physiology
MH  - Proto-Oncogene Proteins c-akt/physiology
MH  - SOXB1 Transcription Factors/analysis/physiology
MH  - Signal Transduction/physiology
MH  - Sodium-Phosphate Cotransporter Proteins, Type IIb/analysis/*physiology
OTO - NOTNLM
OT  - Breast cancer stem cells
OT  - CD147
OT  - PI3K/AKT pathway
OT  - SLC34A2
OT  - SOX2
OT  - stem cell-like phenotypes
EDAT- 2017/04/07 06:00
MHDA- 2017/04/19 06:00
CRDT- 2017/04/07 06:00
AID - 10.1177/1010428317695927 [doi]
PST - ppublish
SO  - Tumour Biol. 2017 Apr;39(4):1010428317695927. doi: 10.1177/1010428317695927.

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