Vacuolar protein sorting-associated protein 72 homolog (VPS72) binding to lysine acetyltransferase 5 (KAT5) promotes the proliferation, invasion and migration of hepatocellular carcinoma through regulating phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT) signaling pathway

Chen, Tiejun; Tu, Yinuo; Lv, Dongnuo; Lin, Kunpeng; Tang, Hui; Huang, Wenjie

doi:10.1080/21655979.2022.2056692

Cited by 8 publications

(6 citation statements)

References 33 publications

(30 reference statements)

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“…In this study, CNV-driven VPS72 overexpression activated the malignant behavior of HCC and exerted a strong prognostic effect on HCC patients. A recent study revealed that VPS72 knockdown inhibited the growth and migration of HCC cells in vitro and inhibited the AKT signaling pathway 33 . However, in our study, overexpression of VPS72 promoted the initiation and progression of an oncogene-induced (AKT/β-catenin) mouse HCC model, and targeting VPS72 inhibited the progression of this HCC model, suggesting that VPS72 is more likely to play a role in promoting HCC progression through pathways other than AKT.…”

Section: Discussioncontrasting

confidence: 79%

Targeting VPS72 inhibits ACTL6A/MYC axis activity in HCC progression

et al. 2023

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Background and Aims: HCC is a highly heterogeneous disease that is caused largely by genomic copy number variations. Herein, the mechanistic and therapeutically targeted role of vacuolar protein sorting 72 homologue (VPS72), a novel copy number variation cis-driven gained gene identified by genome-wide copy number variation and transcriptome analyses in HCC, is not well understood. Approach and Results: First, overexpression of VPS72 enhanced the initiation and progression of HCC in vitro and in vivo. Mechanistically, VPS72 interacted with the oncoproteins MYC and actin-like 6A (ACTL6A) and promoted the formation of the ACTL6A/MYC complex. Furthermore, ACTL6A regulated VPS72 protein stability by weakening the interaction between tripartite motif containing 21 (TRIM21) and VPS72. Thus, the interaction between VPS72 and ACTL6A enhanced the affinity of MYC for its target gene promoters and promoted their transcription, thereby contributing to HCC progression, which was inhibited by adeno-associated virus serotype 8 (AAV8)-mediated short hairpin RNA (shRNA) against VPS72. Conclusions: This study reveals the molecular mechanism of ACTL6A/VPS72/MYC in HCC, providing a theoretical basis and therapeutic target for this malignancy.

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Section: Discussioncontrasting

confidence: 79%

Targeting VPS72 inhibits ACTL6A/MYC axis activity in HCC progression

et al. 2023

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“…Chromatin remodeler CHD7 , a somatic driver candidate in colorectal cancer (CRC), promotes CRC cell growth by binding target gene promoters, encouraging an open chromatin conformation and subsequent transcription, whereas CHD7 knockdown inhibits CRC cell growth [ 74 ]. Similarly, POLR1B knockdown induces lung cancer cell apoptosis [ 75 ], VPS72 knockdown inhibits the proliferation, invasion, and migration of hepatocellular carcinoma (HCC) cells [ 76 ], and UBTF silencing suppresses melanoma cell proliferation [ 77 ]. DPF3 , a chromatin remodeling cofactor significantly downregulated in breast cancer tissue, promoting the proliferation of breast cancer cells, has been suggested as a novel therapeutic target for breast cancer therapy [ 78 ].…”

Section: Discussionmentioning

confidence: 99%

Alterations in the Epigenetic Machinery Associated with Prostate Cancer Health Disparities

Craddock

Jiang

Patrick

et al. 2023

Cancers

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Prostate cancer is driven by acquired genetic alterations, including those impacting the epigenetic machinery. With African ancestry as a significant risk factor for aggressive disease, we hypothesize that dysregulation among the roughly 656 epigenetic genes may contribute to prostate cancer health disparities. Investigating prostate tumor genomic data from 109 men of southern African and 56 men of European Australian ancestry, we found that African-derived tumors present with a longer tail of epigenetic driver gene candidates (72 versus 10). Biased towards African-specific drivers (63 versus 9 shared), many are novel to prostate cancer (18/63), including several putative therapeutic targets (CHD7, DPF3, POLR1B, SETD1B, UBTF, and VPS72). Through clustering of all variant types and copy number alterations, we describe two epigenetic PCa taxonomies capable of differentiating patients by ancestry and predicted clinical outcomes. We identified the top genes in African- and European-derived tumors representing a multifunctional “generic machinery”, the alteration of which may be instrumental in epigenetic dysregulation and prostate tumorigenesis. In conclusion, numerous somatic alterations in the epigenetic machinery drive prostate carcinogenesis, but African-derived tumors appear to achieve this state with greater diversity among such alterations. The greater novelty observed in African-derived tumors illustrates the significant clinical benefit to be derived from a much needed African-tailored approach to prostate cancer healthcare aimed at reducing prostate cancer health disparities.

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“…The Biogrid DataBase (version 4.4; https://thebiogrid.org/ ) is a database that can be used to predict the protein-protein link [ 22 ].…”

Section: Methodsmentioning

confidence: 99%

Far upstream element -binding protein 1 (FUBP1) participates in the malignant process and glycolysis of colon cancer cells by combining with c-Myc

Wang

et al. 2022

Bioengineered

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Human distal upstream element (Fuse) binding protein 1 (FUBP1) is a transcriptional regulator of c-Myc and represents an important prognostic marker in many cancers. Therefore, the present study aimed to investigate whether FUBP1 could combine with c-Myc to participate in the progression of colon cancer. Detection of FUBP1 expression was done through reverse transcription-quantitative PCR (RT-qPCR), and the combination of FUBP1 and c-Myc was detected by immunoprecipitation assay. Cell counting kit (CCK)-8, colony formation, transwell and wound healing were applied for assessing the ability of cells to proliferate, migrate, and invade; glycolysis and lactic acid detection kits were used to detect glucose uptake and lactic acid content, while western blotting was adopted to detect the protein expression of glycolysis-related genes. FUBP1 expression was elevated in HCT116 cells relative to other colon cancer cell lines, and silencing FUBP1 could inhibit the ability of HCT116 cells to proliferate, migrate, invade and glycolysis, and enhance its apoptosis. In addition, the results of immunoprecipitation experiments showed that FUBP1 could bind to c-Myc. c-Myc overexpression reversed the inhibitory effects of FUBP1 knockdown on the ability of HCT116 cells to proliferate, migrate, invade and glycolysis. The results indicated that FUBP1 could participate in the deterioration process of colon cancer cells by combining with c-Myc, and it has clinical significance for understanding the key role of FUBP1 in tumor genesis.

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Vacuolar protein sorting-associated protein 72 homolog (VPS72) binding to lysine acetyltransferase 5 (KAT5) promotes the proliferation, invasion and migration of hepatocellular carcinoma through regulating phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT) signaling pathway

Cited by 8 publications

References 33 publications

Targeting VPS72 inhibits ACTL6A/MYC axis activity in HCC progression

Targeting VPS72 inhibits ACTL6A/MYC axis activity in HCC progression

Alterations in the Epigenetic Machinery Associated with Prostate Cancer Health Disparities

Far upstream element -binding protein 1 (FUBP1) participates in the malignant process and glycolysis of colon cancer cells by combining with c-Myc

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