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Dicer1 dysfunction promotes stemness and aggression in endometrial carcinoma.

Abstract Endometrial carcinoma is one of the most common gynecological malignancies, but the molecular events involved in the development and progression of endometrial carcinoma remain unclear. Dicer1 and cancer stem cells play important roles in cell motility and survival. This study investigated the role of the let-7 family and Dicer1 in the stemness of endometrial carcinoma cells. We profiled Dicer1 expression in clinical samples and explored its relationship with stem cell-associated markers and clinical parameters. We showed that Dicer1 dysfunction leads to the enrichment of tumor stemness features and tumor aggression both in vitro and in vivo. We also identified the mechanism related to this potential tumor-predisposing phenotype: loss of Dicer1 induced abnormal expression of the let-7 family, which comprises well-known tumor suppressors, thus regulating stemness in endometrial carcinoma cells.
PMID
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Authors

Mayor MeshTerms
Keywords

Dicer1

Endometrial carcinoma

let-7

stemness

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




PMID- 28381177
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  - Dicer1 dysfunction promotes stemness and aggression in endometrial carcinoma.
PG  - 1010428317695967
LID - 10.1177/1010428317695967 [doi]
AB  - Endometrial carcinoma is one of the most common gynecological malignancies, but
      the molecular events involved in the development and progression of endometrial
      carcinoma remain unclear. Dicer1 and cancer stem cells play important roles in
      cell motility and survival. This study investigated the role of the let-7 family 
      and Dicer1 in the stemness of endometrial carcinoma cells. We profiled Dicer1
      expression in clinical samples and explored its relationship with stem
      cell-associated markers and clinical parameters. We showed that Dicer1
      dysfunction leads to the enrichment of tumor stemness features and tumor
      aggression both in vitro and in vivo. We also identified the mechanism related to
      this potential tumor-predisposing phenotype: loss of Dicer1 induced abnormal
      expression of the let-7 family, which comprises well-known tumor suppressors,
      thus regulating stemness in endometrial carcinoma cells.
FAU - Wang, Xiao-Jun
AU  - Wang XJ
AD  - 1 Department of Obstetrics and Gynecology, Shanghai First Maternity and Infant
      Health Hospital, Tongji University School of Medicine, Shanghai, China.
AD  - 2 Department of Obstetrics and Gynecology, Shanghai General Hospital, Shanghai
      Jiao Tong University School of Medicine, Shanghai, China.
FAU - Jiang, Fei-Zhou
AU  - Jiang FZ
AD  - 3 Department of Obstetrics and Gynecology, The First Affiliated Hospital of
      Soochow University, Suzhou, China.
FAU - Tong, Huan
AU  - Tong H
AD  - 1 Department of Obstetrics and Gynecology, Shanghai First Maternity and Infant
      Health Hospital, Tongji University School of Medicine, Shanghai, China.
FAU - Ke, Jie-Qi
AU  - Ke JQ
AD  - 2 Department of Obstetrics and Gynecology, Shanghai General Hospital, Shanghai
      Jiao Tong University School of Medicine, Shanghai, China.
FAU - Li, Yi-Ran
AU  - Li YR
AD  - 1 Department of Obstetrics and Gynecology, Shanghai First Maternity and Infant
      Health Hospital, Tongji University School of Medicine, Shanghai, China.
FAU - Zhang, Hui-Lin
AU  - Zhang HL
AD  - 2 Department of Obstetrics and Gynecology, Shanghai General Hospital, Shanghai
      Jiao Tong University School of Medicine, Shanghai, China.
FAU - Yan, Xiao-Fang
AU  - Yan XF
AD  - 2 Department of Obstetrics and Gynecology, Shanghai General Hospital, Shanghai
      Jiao Tong University School of Medicine, Shanghai, China.
FAU - Wang, Fang-Yuan
AU  - Wang FY
AD  - 2 Department of Obstetrics and Gynecology, Shanghai General Hospital, Shanghai
      Jiao Tong University School of Medicine, Shanghai, China.
FAU - Wan, Xiao-Ping
AU  - Wan XP
AD  - 1 Department of Obstetrics and Gynecology, Shanghai First Maternity and Infant
      Health Hospital, Tongji University School of Medicine, Shanghai, 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 (Antigens, CD44)
RN  - 0 (CD44 protein, human)
RN  - 0 (MicroRNAs)
RN  - 0 (Tumor Suppressor Proteins)
RN  - 0 (mirnlet7 microRNA, human)
RN  - EC 3.1.26.3 (DICER1 protein, human)
RN  - EC 3.1.26.3 (Ribonuclease III)
RN  - EC 3.6.4.13 (DEAD-box RNA Helicases)
SB  - IM
MH  - Adult
MH  - Aged
MH  - Animals
MH  - Antigens, CD44/analysis
MH  - Cell Line, Tumor
MH  - DEAD-box RNA Helicases/*physiology
MH  - Endometrial Neoplasms/*pathology
MH  - Female
MH  - Humans
MH  - Mice
MH  - Mice, Inbred BALB C
MH  - MicroRNAs/physiology
MH  - Middle Aged
MH  - Neoplastic Stem Cells/chemistry/physiology
MH  - Ribonuclease III/*physiology
MH  - Tumor Suppressor Proteins/physiology
OTO - NOTNLM
OT  - Dicer1
OT  - Endometrial carcinoma
OT  - let-7
OT  - stemness
EDAT- 2017/04/07 06:00
MHDA- 2017/04/19 06:00
CRDT- 2017/04/07 06:00
AID - 10.1177/1010428317695967 [doi]
PST - ppublish
SO  - Tumour Biol. 2017 Apr;39(4):1010428317695967. doi: 10.1177/1010428317695967.

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