PMID- 31894336
OWN - NLM
STAT- MEDLINE
DCOM- 20200821
LR  - 20211204
IS  - 1791-2431 (Electronic)
IS  - 1021-335X (Linking)
VI  - 43
IP  - 2
DP  - 2020 Feb
TI  - Mechanisms underlying the promotion of osteosarcoma cell proliferation and 
      invasion by lncRNA PBB12.
PG  - 736-746
LID - 10.3892/or.2019.7451 [doi]
AB  - PBB12, a long noncoding RNA (lncRNA), has not been reported to be involved in the 
      progression of osteosarcoma to date. According to our research data, it was found 
      that osteosarcoma patients with a high PBB12 level frequently showed increased 
      metastasis. Mechanistic research demonstrated that PBB12 can competitively bind 
      to hsa‑miR‑204‑5p by acting as a microRNA sponge. Furthermore, PBB12 intervenes 
      in the Kruppel‑like factor 4 (KLF4)/hsa‑miR‑204‑5p/activating transcription 
      factor 2 (ATF2) pathway and affects the proliferation and invasion of 
      osteosarcoma cells. High PBB12 expression was founld to lead to the loss of 
      function of the cancer suppressors KLF4 and hsa‑miR‑204‑5p; these effects are the 
      intrinsic reason why osteosarcoma patients with high levels of PBB12 often 
      develop tumor metastases. In vitro functional experimental data showed that in 
      the osteosarcoma cell lines MG63 and SAOS‑2, PBB12 silencing and overexpression 
      significantly increases or reversed the inhibitory effect of KLF4 on the 
      proliferation and invasion of tumor cells, respectively. The involvement of the 
      interaction between PBB12 and the KLF4/hsa‑miR‑204‑5p/ATF2 pathway in 
      osteosarcoma progression was reported for the first time, and these data provide 
      important theoretical support for gene therapy targeting KLF4 and hsa‑miR‑204‑5p. 
      The great significance of this study is that a high or low genetic background 
      level of PBB12 in osteosarcoma patients may serve as an important marker for 
      screening patients for a high risk of tumor metastasis. Furthermore, for 
      osteosarcoma patients with high PBB12 expression, the primary task for all 
      accurate personalized clinical treatment programs may be the determination of how 
      to effectively knock down PBB12 in tumor bodies.
FAU - Ma, Tianwen
AU  - Ma T
AD  - Department of Orthopedics, Huashan Hospital, Fudan University, Shanghai 200040, 
      P.R. China.
FAU - Liu, Aiping
AU  - Liu A
AD  - Department of Laboratory Medicine, Huashan Hospital, Fudan University, Shanghai 
      200040, P.R. China.
FAU - Xu, Dongwen
AU  - Xu D
AD  - Department of Laboratory Medicine, Huashan Hospital, Fudan University, Shanghai 
      200040, P.R. China.
FAU - Zhang, Tao
AU  - Zhang T
AD  - Department of Laboratory Medicine, Huashan Hospital, Fudan University, Shanghai 
      200040, P.R. China.
LA  - eng
PT  - Journal Article
DEP - 20191231
PL  - Greece
TA  - Oncol Rep
JT  - Oncology reports
JID - 9422756
RN  - 0 (KLF4 protein, human)
RN  - 0 (Kruppel-Like Factor 4)
RN  - 0 (Kruppel-Like Transcription Factors)
RN  - 0 (MIRN204 microRNA, human)
RN  - 0 (MicroRNAs)
RN  - 0 (RNA, Long Noncoding)
SB  - IM
MH  - Adolescent
MH  - Bone Neoplasms/*genetics
MH  - Cell Line, Tumor
MH  - Cell Proliferation
MH  - Child
MH  - Female
MH  - Humans
MH  - Kruppel-Like Factor 4
MH  - Kruppel-Like Transcription Factors/*genetics
MH  - Male
MH  - MicroRNAs/*genetics
MH  - Neoplasm Invasiveness
MH  - Osteosarcoma/*genetics
MH  - RNA, Long Noncoding/*genetics
MH  - *Up-Regulation
MH  - Young Adult
OTO - NOTNLM
OT  - PBB12
OT  - hsa-miR-204-5p
OT  - KLF4
OT  - ATF2
OT  - osteosarcoma
EDAT- 2020/01/03 06:00
MHDA- 2020/08/22 06:00
CRDT- 2020/01/03 06:00
PHST- 2019/08/12 00:00 [received]
PHST- 2019/11/29 00:00 [accepted]
PHST- 2020/01/03 06:00 [pubmed]
PHST- 2020/08/22 06:00 [medline]
PHST- 2020/01/03 06:00 [entrez]
AID - 10.3892/or.2019.7451 [doi]
PST - ppublish
SO  - Oncol Rep. 2020 Feb;43(2):736-746. doi: 10.3892/or.2019.7451. Epub 2019 Dec 31.