scholarly journals Up-regulation and subcellular localization of hnRNP A2/B1 in the development of hepatocellular carcinoma

BMC Cancer ◽  
2010 ◽  
Vol 10 (1) ◽  
Author(s):  
Huaqing Cui ◽  
Feng Wu ◽  
Yanling Sun ◽  
Guocai Fan ◽  
Qingming Wang
Keyword(s):  
Hepatocellular Carcinoma ◽  
Subcellular Localization

scholarly journals Prohibitin 1 in liver injury and cancer

2020 ◽  
Vol 245 (5) ◽  
pp. 385-394 ◽  
Author(s):  
Lucía Barbier-Torres ◽  
Shelly C Lu
Keyword(s):  
Hepatocellular Carcinoma ◽  
Liver Injury ◽  
Subcellular Localization ◽  
Oncogenic Signaling ◽  
Alcoholic Fatty Liver ◽  
Post Translational Modifications ◽  
Cholangiocarcinoma Cell ◽  
Liver Health ◽  
Oncogenic Signaling Pathways ◽  
Prohibitin 1

Prohibitin 1 is an evolutionary conserved and ubiquitously expressed protein that exerts different biological functions depending on its subcellular localization. The role of prohibitin 1 in liver cancer is controversial as it can be pro- or anti-tumorigenic. However, most of the studies to date have described prohibitin 1 primarily as a tumor suppressor in the liver. Its deficiency sensitizes the liver to cholestatic liver injury, non-alcoholic fatty liver disease, inflammatory insults, and cancer. Liver-specific Phb1-knockout mice spontaneously develop hepatocellular carcinoma, Phb1 heterozygotes are more susceptible to develop cholangiocarcinoma, and the majority of human hepatocellular carcinomas and cholangiocarcinomas have reduced prohibitin 1 expression. Consistent with a tumor suppressive role in the liver, prohibitin 1 negatively regulates proliferation in hepatocytes and human hepatocellular carcinoma and cholangiocarcinoma cell lines, and multiple oncogenic signaling pathways are activated when prohibitin 1 is deficient. Although best known as a mitochondrial chaperone, prohibitin 1 can protect the liver by mitochondrial-independent mechanisms. This review summarizes what’s known about prohibitin 1’s role in liver pathology, with the focus on hepatoprotection and carcinogenesis. Impact statement This review summarizes the last decades of research on PHB1 in liver pathobiology. PHB1 is a key player for liver health as it is hepatoprotective and tumor suppressive. We highlight the importance of PHB1’s subcellular localization, post-translational modifications, and interacting proteins as major determinants of PHB1 cytoprotective function and anti-tumor activity in the liver.

Hypocrellin B in hepatocellular carcinoma cells: Subcellular localization and sonodynamic damage

2015 ◽  
Vol 91 (5) ◽  
pp. 399-406 ◽  
Author(s):  
Xinna Wang ◽  
Jianmei Luo ◽  
Albert Wingnang Leung ◽  
Yajun Li ◽  
Hongwei Zhang ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Subcellular Localization ◽  
Carcinoma Cells ◽  
Hepatocellular Carcinoma Cells ◽  
Hypocrellin B ◽  
Sonodynamic Damage

scholarly journals Role of long intergenic non-protein coding RNA 01857 in hepatocellular carcinoma malignancy via the regulation of the microRNA-197-3p/anterior GRadient 2 axis

PLoS ONE ◽  
2021 ◽  
Vol 16 (11) ◽  
pp. e0258312
Author(s):  
Jiangang Bi ◽  
Yusheng Guo ◽  
Qi Li ◽  
Liping Liu ◽  
Shiyun Bao ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cell Proliferation ◽  
Subcellular Localization ◽  
Differential Expression ◽  
Key Factors ◽  
Protein Coding ◽  
Proliferation And Apoptosis

Objective This study investigates the differential expression and the mechanism of long intergenic non-protein coding RNA (LINC) 01857 in hepatocellular carcinoma (HCC) proliferation and apoptosis. Methods LINC01857 expression in HCC tissues and cells was evaluated. In addition, gain-of and loss-of functions were carried out to assess HCC cell proliferation and apoptosis. After that, LINC01857 subcellular localization was predicted and verified. Additionally, the binding relations between LINC01857 and microRNA (miRNA)-197-3p and between miR-197-3p and anterior GRadient 2 (AGR2) were detected and confirmed. Besides, HCC cell proliferation and apoptosis were assessed after silencing LINC01857 or overexpressing AGR2. Next, levels of key factors in the AKT and ERK pathways were measured. Additionally, xenograft transplantation was also conducted to confirm the effect of LINC01857 in HCC. Results LINC01857 was overexpressed in HCC. Silencing LINC01857 leads to a blockage in HCC cell proliferation but improved apoptosis. LINC01857 could competitively bind to miR-197-3p and thus upregulate AGR2. miR-197-3p was poorly expressed in HCC, while AGR2 was overexpressed. Mechanistically, downregulated miR-197-3p or overexpressed AGR2 were observed to attenuate the effect of the LINC01857 knockdown on suppressing cell proliferation and enhancing apoptosis. Moreover, LINC01857 activated the AKT and ERK pathways through the manipulation of the miR-197-3p/AGR2 axis in HCC. Conclusion The results of this study indicated that LINC01857 was highly expressed in HCC, and it could improve HCC cell proliferation and reduce apoptosis via competitively binding to miR-197-3p, promoting AGR2 and upregulating the AKT and ERK pathways.

scholarly journals YAP Subcellular Localization and Hippo Pathway Transcriptome Analysis in Pediatric Hepatocellular Carcinoma

2016 ◽  
Vol 6 (1) ◽  
Author(s):  
Michael J. LaQuaglia ◽  
James L. Grijalva ◽  
Kaly A. Mueller ◽  
Antonio R. Perez-Atayde ◽  
Heung Bae Kim ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Subcellular Localization ◽  
Transcriptome Analysis ◽  
Hippo Pathway

scholarly journals The FKH domain in FOXP3 mRNA frequently contains mutations in hepatocellular carcinoma that influence the subcellular localization and functions of FOXP3

2020 ◽  
Vol 295 (16) ◽  
pp. 5484-5495 ◽  
Author(s):  
Jianwei Ren ◽  
Yi Liu ◽  
Shanshan Wang ◽  
Yu Wang ◽  
Wende Li ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Subcellular Localization ◽  
Genomic Dna ◽  
Target Genes ◽  
Human Cancer ◽  
Luciferase Assay ◽  
Mouse Tumor ◽  
Foxp3 Mrna ◽  
Human Cancer Cell Lines

The transcription factor forkhead box P3 (FOXP3) is a biomarker for regulatory T cells and can also be expressed in cancer cells, but its function in cancer appears to be divergent. The role of hepatocyte-expressed FOXP3 in hepatocellular carcinoma (HCC) is unknown. Here, we collected tumor samples and clinical information from 115 HCC patients and used five human cancer cell lines. We examined FOXP3 mRNA sequences for mutations, used a luciferase assay to assess promoter activities of FOXP3's target genes, and employed mouse tumor models to confirm in vitro results. We detected mutations in the FKH domain of FOXP3 mRNAs in 33% of the HCC tumor tissues, but in none of the adjacent nontumor tissues. None of the mutations occurred at high frequency, indicating that they occurred randomly. Notably, the mutations were not detected in the corresponding regions of FOXP3 genomic DNA, and many of them resulted in amino acid substitutions in the FKH region, altering FOXP3's subcellular localization. FOXP3 delocalization from the nucleus to the cytoplasm caused loss of transcriptional regulation of its target genes, inactivated its tumor-inhibitory capability, and changed cellular responses to histone deacetylase (HDAC) inhibitors. More complex FKH mutations appeared to be associated with worse prognosis in HCC patients. We conclude that mutations in the FKH domain of FOXP3 mRNA frequently occur in HCC and that these mutations are caused by errors in transcription and are not derived from genomic DNA mutations. Our results suggest that transcriptional mutagenesis of FOXP3 plays a role in HCC.

scholarly journals Subcellular Localization of APE1/Ref-1 in Human Hepatocellular Carcinoma: Possible Prognostic Significance

2007 ◽  
Vol 13 (1-2) ◽  
pp. 89-96 ◽  
Author(s):  
Vittorio Di Maso ◽  
Claudio Avellini ◽  
Lory Saveria Crocè ◽  
Natalia Rosso ◽  
Franco Quadrifoglio ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Subcellular Localization ◽  
Prognostic Significance ◽  
Human Hepatocellular Carcinoma

Investigating the functional link between TMEM165 and SPCA1

2019 ◽  
Vol 476 (21) ◽  
pp. 3281-3293 ◽  
Author(s):  
Elodie Lebredonchel ◽  
Marine Houdou ◽  
Hans-Heinrich Hoffmann ◽  
Kateryna Kondratska ◽  
Marie-Ange Krzewinski ◽  
...  
Keyword(s):  
Subcellular Localization ◽  
Complete Loss ◽  
Protein Family ◽  
Uncharacterized Protein ◽  
Functional Link ◽  
P Type

TMEM165 was highlighted in 2012 as the first member of the Uncharacterized Protein Family 0016 (UPF0016) related to human glycosylation diseases. Defects in TMEM165 are associated with strong Golgi glycosylation abnormalities. Our previous work has shown that TMEM165 rapidly degrades with supraphysiological manganese supplementation. In this paper, we establish a functional link between TMEM165 and SPCA1, the Golgi Ca2+/Mn2+ P-type ATPase pump. A nearly complete loss of TMEM165 was observed in SPCA1-deficient Hap1 cells. We demonstrate that TMEM165 was constitutively degraded in lysosomes in the absence of SPCA1. Complementation studies showed that TMEM165 abundance was directly dependent on SPCA1's function and more specifically its capacity to pump Mn2+ from the cytosol into the Golgi lumen. Among SPCA1 mutants that differentially impair Mn2+ and Ca2+ transport, only the Q747A mutant that favors Mn2+ pumping rescues the abundance and Golgi subcellular localization of TMEM165. Interestingly, the overexpression of SERCA2b also rescues the expression of TMEM165. Finally, this paper highlights that TMEM165 expression is linked to the function of SPCA1.

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