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The long non-coding RNA TP73-AS1 modulates HCC cell proliferation through miR-200a-dependent HMGB1/RAGE regulation.

Abstract P73 antisense RNA 1 T (non-protein coding), also known as TP73-AS1, is a long non-coding RNA (lncRNA) which is involved in cell proliferation and the development of tumors. However, the exact effects and molecular mechanisms of TP73-AS1 in hepatocellular carcinoma (HCC) progression are still unknown. The present study is aimed to investigate the detailed functions and the mechanism of TP73-AS1 in regulation of HCC cell proliferation.
PMID
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Authors

Mayor MeshTerms
Keywords

HCC

HMGB1

Proliferation

TP73-AS1

lncRNA

miR-200a

Journal Title journal of experimental & clinical cancer research : cr
Publication Year Start




PMID- 28403886
OWN - NLM
STAT- MEDLINE
DA  - 20170413
DCOM- 20170414
LR  - 20170416
IS  - 1756-9966 (Electronic)
IS  - 0392-9078 (Linking)
VI  - 36
IP  - 1
DP  - 2017 Apr 12
TI  - The long non-coding RNA TP73-AS1 modulates HCC cell proliferation through
      miR-200a-dependent HMGB1/RAGE regulation.
PG  - 51
LID - 10.1186/s13046-017-0519-z [doi]
AB  - BACKGROUND: P73 antisense RNA 1 T (non-protein coding), also known as TP73-AS1,
      is a long non-coding RNA (lncRNA) which is involved in cell proliferation and the
      development of tumors. However, the exact effects and molecular mechanisms of
      TP73-AS1 in hepatocellular carcinoma (HCC) progression are still unknown. The
      present study is aimed to investigate the detailed functions and the mechanism of
      TP73-AS1 in regulation of HCC cell proliferation. METHODS: TP73-AS1 expression in
      HCC tissues and cell lines was determined using real-time PCR assays; the
      correlation of TP73-AS1 expression with clinicopathological features of HCC was
      analyzed. The functions of TP73-AS1 in regulation of HCC cell proliferation was
      evaluated using MTT and BrdU assays. The candidate upstream miRNAs of HMGB1 were 
      screened using miRcode, miRWalk, miRanda and Target scan, verified using
      real-time PCR assays. The interaction between TP73-AS1 and miR-200a was confirmed
      using Luciferase report gene assays. The proten levels of HMGB1 signaling-related
      factors in response to co-processing TP73-AS1 knockdown and miR-200a inhibition
      were determined using Western blot assays and ELISA. Further, miR-200a, HMGB1
      mRNA and RAGE mRNA and their correlations in HCC tissues were determined.
      RESULTS: TP73-AS1 was upregulated in HCC tissues and cell lines. High TP73-AS1
      expression was correlated with worse clinicopathological features, poorer
      prognosis and shorter survival. Knockdown of TP73-AS1 inhibited the HCC
      proliferation and the expression levels of HMGB1, RAGE and NF-kappaB in HCC
      cells. By using online tools, we screened out several candidate upstream miRNAs
      of HMGB1, among which miR-200a overexpression inhibited HMGB1 mRNA expression the
      most significantly. By using luciferase assays, we confirmed that miR-200a could 
      directly bind to TP73-AS1 and the 3'UTR of HMGB1; TP73-AS1 competed with HMGB1
      for miR-200a binding. MiR-200a inhibition could up-regulate HMGB1, RAGE,
      NF-kappaB expression as well as NF-kappaB regulated cytokines levels, which could
      be partially restored by si-TP73-AS1. In HCC tissues, miR-200a was down-regulated
      while HMGB1 and RAGE were up-regulated; TP73-AS1 was inversely correlated with
      miR-200a, while positively correlated with HMGB1 and RAGE, respectively.
      CONCLUSION: Our data indicated that TP73-AS1 might be an oncogenic lncRNA that
      promoted proliferation of HCC and could be regarded as a therapeutic target in
      human HCC.
FAU - Li, Shaling
AU  - Li S
AD  - Hunan Key Laboratory of Viral Hepatitis, Department of Infectious Disease,
      Xiangya Hospital, Central South University, Changsha, 410008, China.
FAU - Huang, Yan
AU  - Huang Y
AD  - Hunan Key Laboratory of Viral Hepatitis, Department of Infectious Disease,
      Xiangya Hospital, Central South University, Changsha, 410008, China.
FAU - Huang, Yun
AU  - Huang Y
AD  - Department of Surgery, Xiangya Hospital, Central South University, Changsha,
      410008, China.
FAU - Fu, Yongming
AU  - Fu Y
AD  - Hunan Key Laboratory of Viral Hepatitis, Department of Infectious Disease,
      Xiangya Hospital, Central South University, Changsha, 410008, China.
FAU - Tang, Daolin
AU  - Tang D
AD  - Department of Surgery, University of Pittsburgh, Pittsburgh, 15260, USA.
FAU - Kang, Rui
AU  - Kang R
AD  - Department of Surgery, University of Pittsburgh, Pittsburgh, 15260, USA.
FAU - Zhou, Rongrong
AU  - Zhou R
AD  - Hunan Key Laboratory of Viral Hepatitis, Department of Infectious Disease,
      Xiangya Hospital, Central South University, Changsha, 410008, China.
      [email protected]
FAU - Fan, Xue-Gong
AU  - Fan XG
AD  - Hunan Key Laboratory of Viral Hepatitis, Department of Infectious Disease,
      Xiangya Hospital, Central South University, Changsha, 410008, China.
      [email protected]
LA  - eng
PT  - Journal Article
DEP - 20170412
PL  - England
TA  - J Exp Clin Cancer Res
JT  - Journal of experimental & clinical cancer research : CR
JID - 8308647
RN  - 0 (Antigens, Neoplasm)
RN  - 0 (HMGB1 Protein)
RN  - 0 (HMGB1 protein, human)
RN  - 0 (MIRN200 microRNA, human)
RN  - 0 (MicroRNAs)
RN  - 0 (NF-kappa B)
RN  - 0 (RNA, Antisense)
RN  - 0 (RNA, Long Noncoding)
RN  - 0 (Tumor Protein p73)
RN  - 0 (p73 protein, human)
RN  - EC 2.7.11.22 (MOK protein, human)
RN  - EC 2.7.11.24 (Mitogen-Activated Protein Kinases)
SB  - IM
MH  - Antigens, Neoplasm/biosynthesis/genetics/*metabolism
MH  - Carcinoma, Hepatocellular/*genetics/metabolism/pathology
MH  - Cell Line, Tumor
MH  - Cell Proliferation/genetics
MH  - Down-Regulation
MH  - Female
MH  - Gene Knockdown Techniques
MH  - HMGB1 Protein/biosynthesis/genetics/*metabolism
MH  - Hep G2 Cells
MH  - Humans
MH  - Liver Neoplasms/*genetics/metabolism/pathology
MH  - Male
MH  - MicroRNAs/*biosynthesis/genetics
MH  - Middle Aged
MH  - Mitogen-Activated Protein Kinases/biosynthesis/genetics/*metabolism
MH  - NF-kappa B/metabolism
MH  - Prognosis
MH  - RNA, Antisense/biosynthesis/*genetics
MH  - RNA, Long Noncoding/biosynthesis/*genetics
MH  - Real-Time Polymerase Chain Reaction
MH  - Tumor Protein p73/biosynthesis/*genetics
PMC - PMC5389141
OTO - NOTNLM
OT  - HCC
OT  - HMGB1
OT  - Proliferation
OT  - TP73-AS1
OT  - lncRNA
OT  - miR-200a
EDAT- 2017/04/14 06:00
MHDA- 2017/04/15 06:00
CRDT- 2017/04/14 06:00
PHST- 2017/01/15 [received]
PHST- 2017/03/28 [accepted]
AID - 10.1186/s13046-017-0519-z [doi]
AID - 10.1186/s13046-017-0519-z [pii]
PST - epublish
SO  - J Exp Clin Cancer Res. 2017 Apr 12;36(1):51. doi: 10.1186/s13046-017-0519-z.

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