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JAK2 variations and functions in lung adenocarcinoma.

Abstract Lung cancer ranks as the first most common cancer and the first leading cause of cancer-related death in China and worldwide. Due to the difficulty in early diagnosis and the onset of cancer metastasis, the 5-year survival rate of lung cancer remains low. JAK2 has emerged as pivotal participant in biological processes, often dysregulated in a range of cancers. Recently our study found that JAK2 might play an important role in lung cancer pathogenesis. While our understanding of JAK2 in the onset and progression of lung cancer is still in its infancy, there is no doubt that understanding the variations and functions of JAK2 will certainly secure strong biomarkers and improve treatment options for lung cancer patients. The expression level of JAK2 mRNA was assayed using RT-PCR. JAK2 mutations and amplification were detected using next-generation sequencing (NGS). The shRNA and overexpression plasmids of JAK2 were conducted. MTT (3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyl-tetrazoliumbromide) assay, Trans-well migration and Matrigel invasion assay were conducted to study the proliferation, migration and invasion abilities of lung adenocarcinoma cells independently. We found that JAK2 mRNA was up-regulated in lung adenocarcinoma tissues when compared with their adjacent non-tumor tissues, and was associated with lymph node metastasis ( p < 0.05). JAK2 V617F and N30S mutations and JAK2 amplification were detected by NGS in plasmid samples in patients with lung adenocarcinoma. Downregulation of JAK2 inhibited the proliferation, migration and invasion abilities of lung adenocarcinoma A549 cells. Moreover, overexpression of JAK2 induced the proliferation, migration and invasion abilities of A549 cells. Thus, the up-regulation, mutation and amplification of JAK2 detected in lung adenocarcinoma may participate in lung cancer progression by regulating cancer cells' proliferation, migration and invasion.
PMID
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Authors

Mayor MeshTerms
Keywords

JAK2

JAK2 V617F

lung adenocarcinoma

next-generation sequencing

non-small-cell lung cancer

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




PMID- 28639892
OWN - NLM
STAT- MEDLINE
DA  - 20170622
DCOM- 20170711
LR  - 20170713
IS  - 1423-0380 (Electronic)
IS  - 1010-4283 (Linking)
VI  - 39
IP  - 6
DP  - 2017 Jun
TI  - JAK2 variations and functions in lung adenocarcinoma.
PG  - 1010428317711140
LID - 10.1177/1010428317711140 [doi]
AB  - Lung cancer ranks as the first most common cancer and the first leading cause of 
      cancer-related death in China and worldwide. Due to the difficulty in early
      diagnosis and the onset of cancer metastasis, the 5-year survival rate of lung
      cancer remains low. JAK2 has emerged as pivotal participant in biological
      processes, often dysregulated in a range of cancers. Recently our study found
      that JAK2 might play an important role in lung cancer pathogenesis. While our
      understanding of JAK2 in the onset and progression of lung cancer is still in its
      infancy, there is no doubt that understanding the variations and functions of
      JAK2 will certainly secure strong biomarkers and improve treatment options for
      lung cancer patients. The expression level of JAK2 mRNA was assayed using RT-PCR.
      JAK2 mutations and amplification were detected using next-generation sequencing
      (NGS). The shRNA and overexpression plasmids of JAK2 were conducted. MTT (3-(4,
      5-dimethylthiazol-2-yl)-2, 5-diphenyl-tetrazoliumbromide) assay, Trans-well
      migration and Matrigel invasion assay were conducted to study the proliferation, 
      migration and invasion abilities of lung adenocarcinoma cells independently. We
      found that JAK2 mRNA was up-regulated in lung adenocarcinoma tissues when
      compared with their adjacent non-tumor tissues, and was associated with lymph
      node metastasis ( p &lt; 0.05). JAK2 V617F and N30S mutations and JAK2 amplification
      were detected by NGS in plasmid samples in patients with lung adenocarcinoma.
      Downregulation of JAK2 inhibited the proliferation, migration and invasion
      abilities of lung adenocarcinoma A549 cells. Moreover, overexpression of JAK2
      induced the proliferation, migration and invasion abilities of A549 cells. Thus, 
      the up-regulation, mutation and amplification of JAK2 detected in lung
      adenocarcinoma may participate in lung cancer progression by regulating cancer
      cells' proliferation, migration and invasion.
FAU - Xu, Yanjun
AU  - Xu Y
AD  - 1 Department of Chemotherapy, Zhejiang Cancer Hospital, Hangzhou, China.
FAU - Jin, Juan
AU  - Jin J
AD  - 2 Department of Cell Biology and Program in Molecular Cell Biology, Zhejiang
      University School of Medicine, Hangzhou, China.
FAU - Xu, Jiawei
AU  - Xu J
AD  - 2 Department of Cell Biology and Program in Molecular Cell Biology, Zhejiang
      University School of Medicine, Hangzhou, China.
FAU - Shao, Yang W
AU  - Shao YW
AD  - 3 Geneseeq Technology Inc., Toronto, ON, Canada.
FAU - Fan, Yun
AU  - Fan Y
AD  - 1 Department of Chemotherapy, Zhejiang Cancer Hospital, Hangzhou, 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  - EC 2.7.10.2 (JAK2 protein, human)
RN  - EC 2.7.10.2 (Janus Kinase 2)
RN  - Adenocarcinoma of lung
SB  - IM
MH  - A549 Cells
MH  - Adenocarcinoma/*genetics/pathology
MH  - Adult
MH  - Aged
MH  - Cell Movement/genetics
MH  - Cell Proliferation/*genetics
MH  - Disease Progression
MH  - Female
MH  - Gene Expression Regulation, Neoplastic
MH  - Humans
MH  - Janus Kinase 2/biosynthesis/*genetics
MH  - Lung Neoplasms/*genetics/pathology
MH  - Lymphatic Metastasis
MH  - Male
MH  - Middle Aged
MH  - Neoplasm Invasiveness/genetics/pathology
OTO - NOTNLM
OT  - JAK2
OT  - JAK2 V617F
OT  - lung adenocarcinoma
OT  - next-generation sequencing
OT  - non-small-cell lung cancer
EDAT- 2017/06/24 06:00
MHDA- 2017/07/14 06:00
CRDT- 2017/06/23 06:00
AID - 10.1177/1010428317711140 [doi]
PST - ppublish
SO  - Tumour Biol. 2017 Jun;39(6):1010428317711140. doi: 10.1177/1010428317711140.