PubTransformer

A site to transform Pubmed publications into these bibliographic reference formats: ADS, BibTeX, EndNote, ISI used by the Web of Knowledge, RIS, MEDLINE, Microsoft's Word 2007 XML.

Splicing factor hnRNPA2B1 contributes to tumorigenic potential of breast cancer cells through STAT3 and ERK1/2 signaling pathway.

Abstract Increasing evidence has indicated that the splicing factor hnRNPA2B1 plays a direct role in cancer development, progression, gene expression, and signal transduction. Previous studies have shown that knocking down hnRNPA2B1 in breast cancer cells induces apoptosis, but the mechanism and other functions of hnRNPA2B1 in breast cancer are unknown. The goal of this study was to investigate the biological function, clinical significance, and mechanism of hnRNPA2B1 in breast cancer. The expression of hnRNPA2B1 in 92 breast cancer and adjacent normal tissue pairs was analyzed by immunohistochemical staining. Stable clones exhibiting knockdown of hnRNPA2B1 via small hairpin RNA expression were generated using RNA interference technology in breast cancer cell lines. The effects of hnRNPA2B1 on cell proliferation were examined by MTT and EdU assay, and cellular apoptosis and the cell cycle were examined by flow cytometry. A nude mouse xenograft model was established to elucidate the function of hnRNPA2B1 in tumorigenesis in vivo. The role of hnRNPA2B1 in signaling pathways was investigated in vitro. Our data revealed that hnRNPA2B1 was overexpressed in breast cancer tissue specimens and cell lines. Knockdown of hnRNPA2B1 reduced breast cancer cell proliferation, induced apoptosis, and prolonged the S phase of the cell cycle in vitro. In addition, hnRNPA2B1 knockdown suppressed subcutaneous tumorigenicity in vivo. On a molecular level, hnRNPA2B1 knockdown decreased signal transducer and activator of transcription 3 and extracellular-signal-regulated kinase 1/2 phosphorylation. We concluded that hnRNPA2B1 promotes the tumorigenic potential of breast cancer cells, MCF-7 and MDA-MB-231, through the extracellular-signal-regulated kinase 1/2 or signal transducer and activator of transcription 3 pathway, which may serve as a target for future therapies.
PMID
Related Publications

Novel sorafenib analogues induce apoptosis through SHP-1 dependent STAT3 inactivation in human breast cancer cells.

Therapeutic effects of signal transducer and activator of transcription 3 siRNA on human breast cancer in xenograft mice.

Stat3-siRNA induces Fas-mediated apoptosis in vitro and in vivo in breast cancer.

Fyn requires HnRNPA2B1 and Sam68 to synergistically regulate apoptosis in pancreatic cancer.

Ribonucleoprotein HNRNPA2B1 interacts with and regulates oncogenic KRAS in pancreatic ductal adenocarcinoma cells.

Authors

Mayor MeshTerms
Keywords

breast cancer

extracellular-signal-regulated kinase 1/2/signal transducer and activator of transcription 3

hnRNPA2B1

signaling pathway

tumorigenic potential

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




PMID- 28351333
OWN - NLM
STAT- MEDLINE
DA  - 20170329
DCOM- 20170407
LR  - 20170407
IS  - 1423-0380 (Electronic)
IS  - 1010-4283 (Linking)
VI  - 39
IP  - 3
DP  - 2017 Mar
TI  - Splicing factor hnRNPA2B1 contributes to tumorigenic potential of breast cancer
      cells through STAT3 and ERK1/2 signaling pathway.
PG  - 1010428317694318
LID - 10.1177/1010428317694318 [doi]
AB  - Increasing evidence has indicated that the splicing factor hnRNPA2B1 plays a
      direct role in cancer development, progression, gene expression, and signal
      transduction. Previous studies have shown that knocking down hnRNPA2B1 in breast 
      cancer cells induces apoptosis, but the mechanism and other functions of
      hnRNPA2B1 in breast cancer are unknown. The goal of this study was to investigate
      the biological function, clinical significance, and mechanism of hnRNPA2B1 in
      breast cancer. The expression of hnRNPA2B1 in 92 breast cancer and adjacent
      normal tissue pairs was analyzed by immunohistochemical staining. Stable clones
      exhibiting knockdown of hnRNPA2B1 via small hairpin RNA expression were generated
      using RNA interference technology in breast cancer cell lines. The effects of
      hnRNPA2B1 on cell proliferation were examined by MTT and EdU assay, and cellular 
      apoptosis and the cell cycle were examined by flow cytometry. A nude mouse
      xenograft model was established to elucidate the function of hnRNPA2B1 in
      tumorigenesis in vivo. The role of hnRNPA2B1 in signaling pathways was
      investigated in vitro. Our data revealed that hnRNPA2B1 was overexpressed in
      breast cancer tissue specimens and cell lines. Knockdown of hnRNPA2B1 reduced
      breast cancer cell proliferation, induced apoptosis, and prolonged the S phase of
      the cell cycle in vitro. In addition, hnRNPA2B1 knockdown suppressed subcutaneous
      tumorigenicity in vivo. On a molecular level, hnRNPA2B1 knockdown decreased
      signal transducer and activator of transcription 3 and
      extracellular-signal-regulated kinase 1/2 phosphorylation. We concluded that
      hnRNPA2B1 promotes the tumorigenic potential of breast cancer cells, MCF-7 and
      MDA-MB-231, through the extracellular-signal-regulated kinase 1/2 or signal
      transducer and activator of transcription 3 pathway, which may serve as a target 
      for future therapies.
FAU - Hu, Ying
AU  - Hu Y
AD  - 1 Breast Disease Center, Southwest Hospital, Third Military Medical University,
      Chongqing, China.
FAU - Sun, Zihan
AU  - Sun Z
AD  - 1 Breast Disease Center, Southwest Hospital, Third Military Medical University,
      Chongqing, China.
FAU - Deng, Jinmu
AU  - Deng J
AD  - 2 Department of Mammary Gland and Thyroid Gland, Chongqing Hospital of
      Traditional Chinese Medicine, Chongqing, China.
FAU - Hu, Baoquan
AU  - Hu B
AD  - 1 Breast Disease Center, Southwest Hospital, Third Military Medical University,
      Chongqing, China.
FAU - Yan, Wenting
AU  - Yan W
AD  - 1 Breast Disease Center, Southwest Hospital, Third Military Medical University,
      Chongqing, China.
FAU - Wei, Hongyi
AU  - Wei H
AD  - 1 Breast Disease Center, Southwest Hospital, Third Military Medical University,
      Chongqing, China.
FAU - Jiang, Jun
AU  - Jiang J
AD  - 1 Breast Disease Center, Southwest Hospital, Third Military Medical University,
      Chongqing, 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 (Heterogeneous-Nuclear Ribonucleoprotein Group A-B)
RN  - 0 (STAT3 Transcription Factor)
RN  - 0 (STAT3 protein, human)
RN  - 0 (hnRNP A2)
SB  - IM
MH  - Animals
MH  - Apoptosis/genetics
MH  - Breast Neoplasms/*genetics/pathology
MH  - Carcinogenesis/*genetics
MH  - Cell Proliferation/genetics
MH  - Female
MH  - Gene Expression Regulation, Neoplastic/genetics
MH  - Heterogeneous-Nuclear Ribonucleoprotein Group A-B/antagonists &
      inhibitors/biosynthesis/*genetics
MH  - Humans
MH  - MAP Kinase Signaling System/genetics
MH  - MCF-7 Cells
MH  - Mice
MH  - STAT3 Transcription Factor/*genetics
MH  - Xenograft Model Antitumor Assays
OTO - NOTNLM
OT  - breast cancer
OT  - extracellular-signal-regulated kinase 1/2/signal transducer and activator of
      transcription 3
OT  - hnRNPA2B1
OT  - signaling pathway
OT  - tumorigenic potential
EDAT- 2017/03/30 06:00
MHDA- 2017/04/08 06:00
CRDT- 2017/03/30 06:00
AID - 10.1177/1010428317694318 [doi]
PST - ppublish
SO  - Tumour Biol. 2017 Mar;39(3):1010428317694318. doi: 10.1177/1010428317694318.

<?xml version="1.0" encoding="UTF-8"?>
<b:Sources SelectedStyle="" xmlns:b="http://schemas.openxmlformats.org/officeDocument/2006/bibliography"  xmlns="http://schemas.openxmlformats.org/officeDocument/2006/bibliography" >
</b:Sources>