Combination therapy of hTERTR and FAM96A for hepatocellular carcinoma through enhancing apoptosis sensitivity

Wang, Wan-peng; Gao, Haiying

doi:10.3892/etm.2017.5505

Cited by 3 publications

(4 citation statements)

References 39 publications

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“…Evidence supports FAM96A as a tumor suppressor in gastrointestinal stromal tumors, showing that FAM96A re-expressed in gastrointestinal stromal tumors induces cell apoptosis and diminishes tumorigenicity [ 18 ]. FAM96A inhibits tumor growth in nude mice, thereby playing an anti-cancer role in hepatocellular carcinoma [ 17 ]. Although there have been no studies on the function of FAM96A in LA, we speculate that FAM96A may play an anticancer role in LA, based on a previous study.…”

Section: Discussionmentioning

confidence: 99%

“…Family with sequence similarity 96 member A (FAM96A) is a protein belonging to the cytosolic Fe/S protein family and plays a crucial role in biological processes. Previous studies have confirmed that FAM96A suppresses tumor growth in both hepatocellular carcinoma [ 17 ] and gastrointestinal stromal tumors [ 18 ] via a proapoptotic process. However, the function of FAM96A in LA has not been elucidated.…”

Section: Introductionmentioning

confidence: 89%

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Evaluation of hsa_circ_0000018/let-7f-5p/ FAM96A axis in lung adenocarcinoma progression

Li,

Zhao,

et al. 2024

Cancer Biomarkers

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BACKGROUND: Circular RNAs (circRNAs) are critical regulators of lung adenocarcinoma (LA) progression. Although a molecular marker targeting hsa_circ_0000018 has been developed and used for diagnosing colon cancer, the role of this circRNA in LA progression has not been explored till now. OBJECTIVES: This study aimed to elucidate the role and regulatory mechanisms of hsa_circ_0000018 in LA progression. METHODS: LA tissues and corresponding adjacent non-tumor tissues were collected from 36 patients to confirm the levels of circRNAs, microRNAs (miRNAs), and messenger RNAs (mRNAs) using quantitative reverse transcriptase-polymerase chain reaction (qRT-PCR). We also cultured two LA cell lines (A549, PC-9), and the human normal lung epithelial cell line BEAS-2B. Cell function experiments were conducted to assess malignancy in LA cells, including proliferation, migration, and invasion, following forced hsa_circ_0000018 expression. The correlation between hsa_circ_0000018, let-7f-5p, and family with sequence similarity 96 member A (FAM96A) was confirmed by using starBase (miRNA-circRNA interaction database), luciferase assay, and western blotting. RESULTS: Expression of hsa_circ_0000018 and FAM96A was reduced, whereas that of let-7f-5p was upregulated in LA. Cell function assays revealed that upregulation of hsa_circ_0000018 had a suppressive effect on the proliferation, migration, and invasion of LA cells. Additionally, hsa_circ_0000018 sponge binds let-7f-5p, resulting in upregulation of FAM96A expression. CONCLUSION: Our data reveal hsa_circ_0000018 as a tumor suppressor in LA that targets the let-7f-5p/FAM96A axis. Our findings enrich the known regulatory network of circRNAs in LA.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 89%

Evaluation of hsa_circ_0000018/let-7f-5p/ FAM96A axis in lung adenocarcinoma progression

Li,

Zhao,

et al. 2024

Cancer Biomarkers

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“…The corresponding genes are involved in physiological process including cell signaling pathways, catabolic processes, and protein translation [11,12]. Five hypermethylated regions were in genes previously associated with cancer (TRAP1, SLC38A3, CHRM1, EDN2, and PROX1), while six hypomethylated regions were in genes previously associated with cancer (NUMBL, ALDH1B1, FTCD, FASTKD2, FAM96A, and ARHGAP15) [20][21][22][23][24][25][26][27][28][29][30]. Five differentially methylated regions were in genes previously found to be associated with obesity and altered metabolic states (TRAP1, SLC38A3, PROX1, ALDH1B1, and FAM96A) [31][32][33][34][35].…”

Section: Differences In Methylation Patterns Of Hepatocellular Carcin...mentioning

confidence: 99%

Differential methylation patterns in lean and obese non-alcoholic steatohepatitis-associated hepatocellular carcinoma

2022

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Background Nonalcoholic fatty liver disease affects about 24% of the world’s population and may progress to nonalcoholic steatohepatitis (NASH), cirrhosis, and hepatocellular carcinoma (HCC). While more common in those that are obese, NASH-HCC can develop in lean individuals. The mechanisms by which HCC develops and the role of epigenetic changes in the context of obesity and normal weight are not well understood. Methods In this study, we used previously generated mouse models of lean and obese HCC using a choline deficient/high trans-fat/fructose/cholesterol diet and a choline supplemented/high trans-fat/fructose/cholesterol diet, respectively, to evaluate methylation differences in HCC progression in lean versus obese mice. Differentially methylated regions were determined using reduced representation bisulfite sequencing. Results A larger number of differentially methylated regions (DMRs) were seen in NASH-HCC progression in the obese mice compared to the non-obese mice. No overlap existed in the DMRs with the largest methylation differences between the two models. In lean NASH-HCC, methylation differences were seen in genes involved with cancer progression and prognosis (including HCC), such as CHCHD2, FSCN1, and ZDHHC12, and lipid metabolism, including PNPLA6 and LDLRAP1. In obese NASH- HCC, methylation differences were seen in genes known to be associated with HCC, including RNF217, GJA8, PTPRE, PSAPL1, and LRRC8D. Genes involved in Wnt-signaling pathways were enriched in hypomethylated DMRs in the obese NASH-HCC. Conclusions These data suggest that differential methylation may play a role in hepatocarcinogenesis in lean versus obese NASH. Hypomethylation of Wnt signaling pathway-related genes in obese mice may drive progression of HCC, while progression of HCC in lean mice may be driven through other signaling pathways, including lipid metabolism.

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“…Subsequent studies have found that the fusion protein of human telomerase reverse transcriptase receptor (hTERTR) and FAM96A can speci cally bind to hTERT and Apaf-1, respectively, induce apoptosis and further improve the apoptosis sensitivity of liver cancer cells, and thus to inhibit the liver cancer cell proliferation, migration and invasion [16]. Moreover, hTERT-FAM96A combination can also promote cytotoxic T lymphocyte reaction, release of interferon-γ and in ammatory in ltration of T lymphocytes, thus enhancing the toxic effect on liver cancer cells [17]. Above all, hTERT-FAM96A fusion protein may be an effective anti-tumor inhibitor.…”

Section: Introductionmentioning

confidence: 99%

FAM96A and FAM96B Suppress Breast Cancer Proliferation and Migration via the Wnt/β-Catenin Signaling Pathway

Zhang

Sun

Liang

et al. 2021

Preprint

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Background: Family with sequence similarity 96 member A and B (FAM96A and FAM96B) are two highly conserved homologous proteins belonging to MIP18 family. Many studies have shown that FAM96A and FAM96B play many different functions mainly through interacting with other different proteins. Recently, several studies show that FAM96A and FAM96B are significantly down-regulated compared in human gastrointestinal stromal tumors, colon cancer, liver cancer and gastric cancer with corresponding normal tissues. However, the molecular regulatory mechanisms of FAM96A and FAM96B in breast cancer development and metastasis are still unclear. In this work, we aimed to explore the molecular mechanisms of FAM96A and FAM96B in breast cancer progression.Methods: We used specific siRNAs to down-regulate FAM96A and FAM96B expression, and used recombinant plasmids to up-regulate FAM96A and FAM96B expression in breast cancer cells. Cell proliferation was measured using MTT and colony formation assays. Cell cycle and apoptosis were detected by flow cytometry analysis. Wound healing and transwell assays were used to examine cell migration and invasion abilities. The relationships among FAM96A/B, EMT and Wnt/β-catenin signaling pathway were determined by analyzing the expression changes of classical markers and biological functional changes after XAV-939 inhibitor treatment. Results: We found that FAM96A and FAM96B expression in breast cancer was down-regulated. FAM96A/B overexpression suppressed breast cancer cell proliferation, invasion and migration, induced cell apoptosis and led to cell cycle arrested in G0/G1 phase. Conversely, FAM96A/B knockdown exhibited the opposite effects on breast cancer cells. Moreover, our data demonstrated that FAM96A/B overexpression suppressed EMT and Wnt/β-catenin signaling pathway, while FAM96A/B knockdown showed the promoting effects on EMT and Wnt/β-catenin signaling pathway in breast cancer cells. Furthermore, a Wnt pathway inhibitor, XAV-939 treatment reversed the promoting effects of FAM96A and FAM96B knockdown on breast cancer cell proliferation, invasion and migration.Conclusions: Our findings revealed that FAM96A and FAM96B may act as tumor suppressor genes and inhibit breast cancer progression via modulating the Wnt/β-catenin pathway, which can provide the potential markers for the diagnosis and treatment of breast cancer.

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Combination therapy of hTERTR and FAM96A for hepatocellular carcinoma through enhancing apoptosis sensitivity

Cited by 3 publications

References 39 publications

Evaluation of hsa_circ_0000018/let-7f-5p/ FAM96A axis in lung adenocarcinoma progression

Evaluation of hsa_circ_0000018/let-7f-5p/ FAM96A axis in lung adenocarcinoma progression

Differential methylation patterns in lean and obese non-alcoholic steatohepatitis-associated hepatocellular carcinoma

FAM96A and FAM96B Suppress Breast Cancer Proliferation and Migration via the Wnt/β-Catenin Signaling Pathway

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