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Downregulation of microRNA-181d had suppressive effect on pancreatic cancer development through inverse regulation of KNAIN2.

Abstract We explored the expression and function of miR-181d (microRNA-181d) in human pancreatic cancer. Quantitative real-time polymerase chain reaction was used to probe miR-181d expression in both pancreatic cancer cell lines and human pancreatic carcinoma. Pancreatic cancer cell lines, PANC-1 and AsPC-1 cells, were engineered to stably downregulate endogenous miR-181d through lentiviral transduction. The mechanistic effects of miR-181d downregulation on pancreatic cancer development were tested by proliferation, migration, fluorouracil chemosensitivity assays in vitro, and explant assay in vivo. Possible miR-181d downstream gene, NKAIN2 (Na+/K+ transporting ATPase interacting 2), was tested by dual-luciferase activity assay and quantitative real-time polymerase chain reaction. Functional involvement of NKAIN2 in miR-181d-regulated pancreatic cancer development was tested by small interfering RNA-mediated NKAIN2 knockdown in miR-181d-downregulated PANC-1 and AsPC-1 cells. MiR-181d was upregulated in both pancreatic cancer cell lines and human pancreatic carcinoma. Lentivirus-induced miR-181d downregulation decreased pancreatic cancer proliferation, migration, and fluorouracil resistance in vitro and inhibited the growth of cancer explant in vivo. NKAIN2 was directly targeted by miR-181d in pancreatic cancer. Small interfering RNA-mediated NKAIN2 knockdown reversed the inhibition of miR-181d downregulation on pancreatic cancer development. MiR-181d is aberrantly overexpressed in pancreatic cancer. Inhibiting miR-181d may suppress pancreatic cancer development, possibly through the inverse regulation on NKAIN2.
PMID
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Authors

Mayor MeshTerms
Keywords

NKAIN2

Pancreatic cancer

fluorouracil

miR-181d

migration

proliferation

xenograft

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




PMID- 28381166
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  - Downregulation of microRNA-181d had suppressive effect on pancreatic cancer
      development through inverse regulation of KNAIN2.
PG  - 1010428317698364
LID - 10.1177/1010428317698364 [doi]
AB  - We explored the expression and function of miR-181d (microRNA-181d) in human
      pancreatic cancer. Quantitative real-time polymerase chain reaction was used to
      probe miR-181d expression in both pancreatic cancer cell lines and human
      pancreatic carcinoma. Pancreatic cancer cell lines, PANC-1 and AsPC-1 cells, were
      engineered to stably downregulate endogenous miR-181d through lentiviral
      transduction. The mechanistic effects of miR-181d downregulation on pancreatic
      cancer development were tested by proliferation, migration, fluorouracil
      chemosensitivity assays in vitro, and explant assay in vivo. Possible miR-181d
      downstream gene, NKAIN2 (Na+/K+ transporting ATPase interacting 2), was tested by
      dual-luciferase activity assay and quantitative real-time polymerase chain
      reaction. Functional involvement of NKAIN2 in miR-181d-regulated pancreatic
      cancer development was tested by small interfering RNA-mediated NKAIN2 knockdown 
      in miR-181d-downregulated PANC-1 and AsPC-1 cells. MiR-181d was upregulated in
      both pancreatic cancer cell lines and human pancreatic carcinoma.
      Lentivirus-induced miR-181d downregulation decreased pancreatic cancer
      proliferation, migration, and fluorouracil resistance in vitro and inhibited the 
      growth of cancer explant in vivo. NKAIN2 was directly targeted by miR-181d in
      pancreatic cancer. Small interfering RNA-mediated NKAIN2 knockdown reversed the
      inhibition of miR-181d downregulation on pancreatic cancer development. MiR-181d 
      is aberrantly overexpressed in pancreatic cancer. Inhibiting miR-181d may
      suppress pancreatic cancer development, possibly through the inverse regulation
      on NKAIN2.
FAU - Zhang, Guopeng
AU  - Zhang G
AD  - 1 Department of Nuclear Medicine, Tongji Hospital of Tongji Medical College,
      Huazhong University of Science and Technology, Wuhan, China.
FAU - Liu, Dongbo
AU  - Liu D
AD  - 2 Department of Oncology, Affiliated Tongji Hospital of Tongji Medical College,
      Huazhong University of Science and Technology, Wuhan, China.
FAU - Long, Guoxian
AU  - Long G
AD  - 2 Department of Oncology, Affiliated Tongji Hospital of Tongji Medical College,
      Huazhong University of Science and Technology, Wuhan, China.
FAU - Shi, Lei
AU  - Shi L
AD  - 2 Department of Oncology, Affiliated Tongji Hospital of Tongji Medical College,
      Huazhong University of Science and Technology, Wuhan, China.
FAU - Qiu, Hong
AU  - Qiu H
AD  - 2 Department of Oncology, Affiliated Tongji Hospital of Tongji Medical College,
      Huazhong University of Science and Technology, Wuhan, China.
FAU - Hu, Guangyuan
AU  - Hu G
AD  - 2 Department of Oncology, Affiliated Tongji Hospital of Tongji Medical College,
      Huazhong University of Science and Technology, Wuhan, China.
FAU - Hu, Guoqing
AU  - Hu G
AD  - 2 Department of Oncology, Affiliated Tongji Hospital of Tongji Medical College,
      Huazhong University of Science and Technology, Wuhan, China.
FAU - Liu, Shunfang
AU  - Liu S
AD  - 2 Department of Oncology, Affiliated Tongji Hospital of Tongji Medical College,
      Huazhong University of Science and Technology, Wuhan, 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 (MIrn181 microRNA, human)
RN  - 0 (Membrane Proteins)
RN  - 0 (MicroRNAs)
RN  - 0 (NKAIN2 protein, human)
SB  - IM
MH  - Cell Line, Tumor
MH  - Down-Regulation
MH  - Gene Expression Regulation, Neoplastic
MH  - Genes, Tumor Suppressor/*physiology
MH  - Humans
MH  - Membrane Proteins/genetics/*physiology
MH  - MicroRNAs/antagonists & inhibitors/*physiology
MH  - Pancreatic Neoplasms/*etiology/prevention & control
OTO - NOTNLM
OT  - NKAIN2
OT  - Pancreatic cancer
OT  - fluorouracil
OT  - miR-181d
OT  - migration
OT  - proliferation
OT  - xenograft
EDAT- 2017/04/07 06:00
MHDA- 2017/04/19 06:00
CRDT- 2017/04/07 06:00
AID - 10.1177/1010428317698364 [doi]
PST - ppublish
SO  - Tumour Biol. 2017 Apr;39(4):1010428317698364. doi: 10.1177/1010428317698364.

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