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Gene. 2017 Jan 6. pii: S0378-1119(17)30004-5. doi: 10.1016/j.gene.2017.01.004. [Epub ahead of print]

Long noncoding RNA HULC promotes cell proliferation by regulating PI3K/AKT signaling pathway in chronic myeloid leukemia.

Author information

  • 1Department of Hematology, Affiliated Hospital of Guizhou Medical University, Hematopoietic Stem Cell Transplant Center of Guizhou, Blood Diseases Diagnosis and Treatment Center of Guizhou, Guizhou 550001, China.. Electronic address: Yinghaolu123@163.com.
  • 2Department of Hematology, Affiliated Hospital of Guizhou Medical University, Hematopoietic Stem Cell Transplant Center of Guizhou, Blood Diseases Diagnosis and Treatment Center of Guizhou, Guizhou 550001, China.. Electronic address: Yanlimed@126.com.
  • 3Department of Hematology, Affiliated Hospital of Guizhou Medical University, Hematopoietic Stem Cell Transplant Center of Guizhou, Blood Diseases Diagnosis and Treatment Center of Guizhou, Guizhou 550001, China.. Electronic address: xiaochaixc@yeah.net.
  • 4Department of Hematology, Affiliated Hospital of Guizhou Medical University, Hematopoietic Stem Cell Transplant Center of Guizhou, Blood Diseases Diagnosis and Treatment Center of Guizhou, Guizhou 550001, China.. Electronic address: qiankang1@outlook.com.
  • 5Department of Hematology, Affiliated Hospital of Guizhou Medical University, Hematopoietic Stem Cell Transplant Center of Guizhou, Blood Diseases Diagnosis and Treatment Center of Guizhou, Guizhou 550001, China.. Electronic address: pengzhao-1@outlook.com.
  • 6Department of Hematology, Affiliated Hospital of Guizhou Medical University, Hematopoietic Stem Cell Transplant Center of Guizhou, Blood Diseases Diagnosis and Treatment Center of Guizhou, Guizhou 550001, China.. Electronic address: jiexiong_vip@21CN.com.
  • 7Department of Hematology, Affiliated Hospital of Guizhou Medical University, Hematopoietic Stem Cell Transplant Center of Guizhou, Blood Diseases Diagnosis and Treatment Center of Guizhou, Guizhou 550001, China.. Electronic address: Jishiwangedu@outlook.com.

Abstract

Aberrant expression of long noncoding RNA (lncRNA) HULC is associated with various human cancers. However, the role of HULC in chronic myeloid leukemia (CML) is unknown. In this study, we found that HULC was remarkably overexpressed in both leukemia cell lines and primary hematopoietic cells derived from CML patients. The increase in HULC expression was positively correlated with clinical stages in CML. Moreover, the knockdown of HULC significantly inhibited CML cell proliferation and induced apoptosis by repressing c-Myc and Bcl-2. Furthermore, inhibition of HULC enhanced imatinib-induced apoptosis of CML cells. Further experiments demonstrated that HULC silencing markedly suppressed the phosphorylation of PI3K and AKT, indicating that enhancement of imatinib-induced apoptosis by HULC inhibition is related with the reduction of c-Myc expression and inhibition of PI3K/Akt pathway activity. Furthermore, HULC could modulate c-Myc and Bcl-2 by miR-200a as an endogenous sponge. Taken together, these results reveal that HULC promotes oncogenesis in CML and suggest a potential strategy for the CML treatment.

KEYWORDS:

C-MYC; CML; HULC; LncRNA; PI3K/AKT; miR-200a

PMID:
28069548
DOI:
10.1016/j.gene.2017.01.004
[PubMed - as supplied by publisher]
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