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Long non-coding RNA HULC promotes tumor angiogenesis in liver cancer by up-regulating sphingosine kinase 1 (SPHK1)
TLDR
HULC promotes tumor angiogenesis in liver cancer through miR-107/E2F1/SPHK1 signaling through complementary base pairing, which provides new insights into the mechanism of tumorAngiogenesis.
Global mapping of CARM1 substrates defines enzyme specificity and substrate recognition
TLDR
It is demonstrated that the N-terminus of CARM1 is involved in substrate recognition and nearly indispensable for substrate methylation, and proposed that development ofCARM1-specific inhibitors should focus on its N- terminus.
MiR-506 suppresses proliferation of hepatoma cells through targeting YAP mRNA 3′UTR
TLDR
MiR-506 suppresses the proliferation of hepatoma cells by targeting YAP mRNA, which is a miRNA involved in carcinogenesis of several kinds of cancer.
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.
Oncoprotein HBXIP Modulates Abnormal Lipid Metabolism and Growth of Breast Cancer Cells by Activating the LXRs/SREBP-1c/FAS Signaling Cascade.
TLDR
It is concluded that the oncoprotein HBXIP contributes to the abnormal lipid metabolism in breast cancer through LXRs/SREBP-1c/FAS signaling, providing new insights into the mechanisms by which cancer cells reprogram lipid metabolismIn their favor.
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.
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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