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Elevation of Highly Up-regulated in Liver Cancer (HULC) by Hepatitis B Virus X Protein Promotes Hepatoma Cell Proliferation via Down-regulating p18*
TLDR
It is concluded that the up-regulated HULC by HBx promotes proliferation of hepatoma cells through suppressing p18, which provides new insight into the roles of lncRNAs in HBx-related hepatocarcinogenesis.
Hepatitis B virus X protein modulates oncogene yes‐associated protein by CREB to promote growth of hepatoma cells
TLDR
YAP is a key driver gene in HBx‐induced hepatocarcinogenesis in a CREB‐dependent manner and may serve as a novel target in HBV‐associated HCC therapy.
Hepatitis B virus X protein mutant HBxΔ127 promotes proliferation of hepatoma cells through up-regulating miR-215 targeting PTPRT.
TLDR
This study identified that protein tyrosine phosphatase, receptor type T (PTPRT) was one of the target genes of miR-215 through targeting 3'UTR of PTPRT mRNA and was able to promote the proliferation of hepatoma cells.
Hepatitis B virus X protein inhibits tumor suppressor miR-205 through inducing hypermethylation of miR-205 promoter to enhance carcinogenesis.
TLDR
HBx is able to inhibit tumor suppressor miR-205 to enhance hepatocarcinogenesis through inducing hypermethylation of miR -205 promoter during their interaction, suggesting that miR_205 is a potential tumor-suppressive gene in HCC.
Hepatitis B virus X protein upregulates oncogene Rab18 to result in the dysregulation of lipogenesis and proliferation of hepatoma cells.
TLDR
The oncogene Rab18, a member of Ras family, enhances the HBx-induced hepatocarcinogenesis through inducing dysregulation of lipogenesis and proliferation of hepatoma cells through two pathways, involving two pathways such as HBx/COX-2/5-LOX/AP-1/CREB/Rab18 andHBx/miR-429/ Rab18.
The oncoprotein hepatitis B X-interacting protein promotes the migration of ovarian cancer cells through the upregulation of S-phase kinase-associated protein 2 by Sp1.
TLDR
It is observed that the overexpression of HBXIP enhanced the migration of ovarian cancer cells, while Skp2 siRNAs decreased the cell migration enhanced byHBXIP.
The oncoprotein HBXIP up-regulates Skp2 via activating transcription factor E2F1 to promote proliferation of breast cancer cells.
TLDR
It is concluded that HBXIP up-regulates Skp2 via activating E2F1 to promote proliferation of breast cancer cells.
Loss of Dnmt3a and endogenous KrasG12D/+ cooperate to regulate hematopoietic stem and progenitor cell functions in leukemogenesis
TLDR
The results suggest that DNMT3A mutations and oncogenic RAS cooperate to regulate hematopoietic stem and progenitor cells and promote myeloid malignancies in leukemogenesis.
The Oncoprotein HBXIP Uses Two Pathways to Up-regulate S100A4 in Promotion of Growth and Migration of Breast Cancer Cells*
TLDR
HBXIP up-regulates S 100A4 through activating S100A4 promoter involving STAT4 and inducing PTEN/PI3K/AKT signaling to promote growth and migration of breast cancer cells.
The oncoprotein HBXIP enhances angiogenesis and growth of breast cancer through modulating FGF8 and VEGF.
TLDR
It is shown that hepatitis B X-interacting protein enhances angiogenesis and growth of breast cancer through modulating FGF8 and VEGF and provides new insights into the mechanism of tumorAngiogenesis in breast cancer.
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