The Roles of Protein Tyrosine Phosphatases in Hepatocellular Carcinoma

Huang, Yide; Zhang, Yafei; Ge, Lilin; Lin, Yao; Kwok, Hang Fai

doi:10.3390/cancers10030082

Cited by 37 publications

(47 citation statements)

References 177 publications

(221 reference statements)

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“…PRL-1-This phosphatase causes activation of AKT, and inhibition of GSK3β, consequently, contributes for elevated levels of Snail expression and decreased Ecadherin expression. In agreement, the high level of this enzyme was associated with more aggressive phenotype and poorer prognosis in hepatocellular carcinoma patients [46].…”

Section: Ptps Contribute For Metastasis Through Extracellular Matrix supporting

confidence: 64%

“…PRL-3-PRL-3 activates the PI3K/PKB pathway and promotes EMT by decreasing PTEN protein expression [23]. In addition, it was demonstrated that expression of PRL-3 in hepatocellular carcinoma patients was positively correlated with the expression of MMPs 1, 9, 10, and 12 [46].…”

Section: Ptps Contribute For Metastasis Through Extracellular Matrix mentioning

confidence: 99%

“…This effect might be one of the explanations in which DUSP1 promotes cancer cells escaping from apoptosis. Indeed, it has been reported that DUSP1 is involved in many cancers: gastric intestinal, lung, breast, squamous cell carcinoma, and head and neck [46]. LMWPTP-Our group has reported that in chemoresistant human chronic myeloid leukemia cells (Lucena-1), LMWPTP is around 20-fold more active than in their sensitive counterpart (K562).…”

Section: Ptps Favor Tumor Growth Through Survival Positive Regulationmentioning

confidence: 99%

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Protein Tyrosine Phosphatases in Tumor Progression and Metastasis: Promoter or Protection?

Ferreira-Halder¹,

Clerici²,

Faria³

et al. 2020

Tumor Progression and Metastasis

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Reversible phosphorylation of proteins, executed by kinases and phosphatases, is the major posttranslational protein modification in eukaryotic cells, causing them to become activated or deactivated. This intracellular event represents a critical regulatory mechanism of several signaling pathways and can be related to a broad number of diseases, including cancer. Few decades ago, protein tyrosine phosphatases (PTPs) were considered as tumor suppressors. However, nowadays, accumulating evidence demonstrates that a misregulation of PTP activities plays a crucial and decisive role in cancer progression and metastasis. In this chapter, we will focus on the molecular aspects that support the crucial role of PTPs in cancer and in turn make them promising for prediction, monitoring, and rational appropriate therapy selection of individual patients.

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Section: Ptps Contribute For Metastasis Through Extracellular Matrix supporting

confidence: 64%

Section: Ptps Contribute For Metastasis Through Extracellular Matrix mentioning

confidence: 99%

Section: Ptps Favor Tumor Growth Through Survival Positive Regulationmentioning

confidence: 99%

See 1 more Smart Citation

Protein Tyrosine Phosphatases in Tumor Progression and Metastasis: Promoter or Protection?

Ferreira-Halder¹,

Clerici²,

Faria³

et al. 2020

Tumor Progression and Metastasis

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“…Hepatocellular carcinoma (HCC), accounting for nearly 90% of liver cancer, is the main form of liver cancer [2,3]. Due to its poor early diagnosis and limited therapy methods, HCC is the most lethal malignant cancer worldwide [4]. Generally, the 5-year overall survival rate of HCC patients is still low [5,6].…”

Section: Introductionmentioning

confidence: 99%

KIF15 Promotes Proliferation and Growth of Hepatocellular Carcinoma

Sun

Shi

et al. 2020

Analytical Cellular Pathology

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Liver cancer is thought as the most common human malignancy worldwide, and hepatocellular carcinoma (HCC) accounts for nearly 90% liver cancer. Due to its poor early diagnosis and limited treatment, HCC has therefore become the most lethal malignant cancers in the world. Recently, molecular targeted therapies showed great promise in the treatment of HCC, and novel molecular therapeutic targets is urgently needed. KIF15 is a microtubule-dependent motor protein involved in multiple cell processes, such as cell division. Additionally, KIF15 has been reported to participate in the growth of various types of tumors; however, the relation between KIF15 and HCC is unclear. Herein, our study investigated the possible role of KIF15 on the progression of HCC and found that KIF15 has high expression in tumor samples from HCC patients. KIF15 could play a critical role in the regulation of cell proliferation of HCC, which was proved by in vitro and in vivo assays. In conclusion, this study confirmed that KIF15 could be a novel therapeutic target for the treatment of HCC.

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“…Previous studies have revealed that deregulation of phosphatases contributes to tumorigenesis and progression of HCC [3][4] . Because of the relative feasibility of developing small molecule inhibitors to block phosphatases 5 , studies focus on the role of such phosphatases may provide clinical significance for the management of HCC. Our previous studies have reported a series of phosphatases that play important roles in HCC.…”

Section: Introductionmentioning

confidence: 99%

INPP5F translocates into cytoplasm and interacts with ASPH to promote tumor growth in hepatocellular carcinoma

Zhou¹,

Lin²,

Liu³

et al. 2020

Preprint

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Background Increasing evidence has suggested inositol polyphosphate 5-phosphatase family contributes to tumorigenesis and tumor progression. However, the role of INPP5F in hepatocellular carcinoma (HCC) and its underlying mechanisms is unclear. Methods The expression of INPP5F in HCC was analyzed in public databases and our clinical specimens. The biological functions of INPP5F were investigated in vitro and vivo. The molecular mechanism of INPP5F in regulating tumor growth were studied by transcriptome-sequencing analysis, mass spectrometry analysis, immunoprecipitation assay and immunofluorescence assay. Results High expression of INPP5F was found in HCC tissues and was associated with poor prognosis in HCC patients. Overexpression of INPP5F promoted HCC cell proliferation, and vice versa. Knockdown of INPP5F suppressed tumor growth in vivo. Results from transcriptome-sequencing analysis showed INPP5F not only regulated a series of cell cycle related genes expression (c-MYC and cyclin E1), but also promoted many aerobic glycolysis related genes expression. Further study confirmed that INPP5F could enhance lactate production and glucose consumption in HCC cells. Mechanistically, INPP5F interacted with ASPH through which INPP5F activated Notch signaling and subsequently promoted the expression of c-MYC and cyclin E1. Interestingly, INPP5F was commonly nuclear-located in cells of adjacent tissues, while cytoplasmic-located was more common in HCC cells. LMB (nuclear export inhibitor) treatment restricted INPP5F in nucleus and was associated with inhibition of Notch signaling and cell proliferation. Furthermore, sequence of nuclear localization signals (NLSs) and nuclear export signals (NESs) in INPP5F aminoacidic sequence were identified. Alteration of the NLSs or NESs influenced the localization of INPP5F and the expression of its downstream molecules. Conclusion These findings indicate that INPP5F functions as an oncogene in HCC via a translocation mechanism and activating ASPH-mediated Notch signaling pathway. INPP5F may serve as a potential therapeutic target for HCC patients.

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The Roles of Protein Tyrosine Phosphatases in Hepatocellular Carcinoma

Cited by 37 publications

References 177 publications

Protein Tyrosine Phosphatases in Tumor Progression and Metastasis: Promoter or Protection?

Protein Tyrosine Phosphatases in Tumor Progression and Metastasis: Promoter or Protection?

KIF15 Promotes Proliferation and Growth of Hepatocellular Carcinoma

INPP5F translocates into cytoplasm and interacts with ASPH to promote tumor growth in hepatocellular carcinoma

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