Over-Expression and Prognostic Significance of FATP5, as a New Biomarker, in Colorectal Carcinoma

Geng, Qishun; Yang, Meng; Li, Lifeng; Shen, Zhibo; Wang, Longhao; Zheng, Yuanyuan; Xue, Wenhua; Zhao, Jie

doi:10.3389/fmolb.2021.770624

Cited by 4 publications

(5 citation statements)

References 35 publications

(32 reference statements)

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“…However, future work should explore the therapeutic benefits of blocking other modes of fatty acid transport. While downregulation of other fatty acid transporters, such as FATP1 and FATP4, did not improve the sensitivity of ACM-treated cells to OV infection in our models (Supplementary Figures 7A, B), there are many other membrane-associated putative fatty acid carriers that display increased expression in cancer cells, including FATPs other than FATP2, the fatty acid translocase CD36 and fatty acid binding proteins (FABPs) (59)(60)(61). Notably, CD36 has demonstrated roles in potentiating tumor growth and anticancer treatment resistance by facilitating the transport FA substrates in the tumor microenvironment (62)(63)(64).…”

mentioning

confidence: 77%

Fatty acid transport protein inhibition sensitizes breast and ovarian cancers to oncolytic virus therapy via lipid modulation of the tumor microenvironment

et al. 2023

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IntroductionAdipocytes in the tumour microenvironment are highly dynamic cells that have an established role in tumour progression, but their impact on anti-cancer therapy resistance is becoming increasingly difficult to overlook.MethodsWe investigated the role of adipose tissue and adipocytes in response to oncolytic virus (OV) therapy in adipose-rich tumours such as breast and ovarian neoplasms.ResultsWe show that secreted products in adipocyte-conditioned medium significantly impairs productive virus infection and OV-driven cell death. This effect was not due to the direct neutralization of virions or inhibition of OV entry into host cells. Instead, further investigation of adipocyte secreted factors demonstrated that adipocyte-mediated OV resistance is primarily a lipid-driven phenomenon. When lipid moieties are depleted from the adipocyte-conditioned medium, cancer cells are re-sensitized to OV-mediated destruction. We further demonstrated that blocking fatty acid uptake by cancer cells, in a combinatorial strategy with virotherapy, has clinical translational potential to overcome adipocyte-mediated OV resistance.DiscussionOur findings indicate that while adipocyte secreted factors can impede OV infection, the impairment of OV treatment efficacy can be overcome by modulating lipid flux in the tumour milieu.

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confidence: 77%

Fatty acid transport protein inhibition sensitizes breast and ovarian cancers to oncolytic virus therapy via lipid modulation of the tumor microenvironment

et al. 2023

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“…RNA isolation and RT–qPCR analysis were carried out according to previous studies ( 20 ). β-actin served as an internal control.…”

Section: Methodsmentioning

confidence: 99%

“…Protein extraction and Western blot analysis were carried out according to previous studies ( 20 ). The primary antibodies included rabbit anti-IGF2BP3 (1:1000, Proteintech, Chicago, USA), anti-CCNB1 (1:1000, Shanghai, China) and anti-C-Myc (1:2,000, Cell Signaling Technology, Beverly, MA, USA).…”

Section: Methodsmentioning

confidence: 99%

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Diagnostic gene signatures and aberrant pathway activation based on m6A methylation regulators in rheumatoid arthritis

et al. 2022

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PurposeRheumatoid arthritis (RA) is a chronic autoimmune disease (AD) characterized by persistent synovial inflammation, bone erosion and progressive joint destruction. This research aimed to elucidate the potential roles and molecular mechanisms of N6-methyladenosine (m6A) methylation regulators in RA.MethodsAn array of tissues from 233 RA and 126 control samples was profiled and integrated for mRNA expression analysis. Following quality control and normalization, the cohort was split into training and validation sets. Five distinct machine learning feature selection methods were applied to the training set and validated in validation sets.ResultsAmong the six models, the LASSO_λ-1se model not only performed better in the validation sets but also exhibited more stringent performance. Two m6A methylation regulators were identified as significant biomarkers by consensus feature selection from all four methods. IGF2BP3 and YTHDC2, which are differentially expressed in patients with RA and controls, were used to predict RA diagnosis with high accuracy. In addition, IGF2BP3 showed higher importance, which can regulate the G2/M transition to promote RA-FLS proliferation and affect M1 macrophage polarization.ConclusionThis consensus of multiple machine learning approaches identified two m6A methylation regulators that could distinguish patients with RA from controls. These m6A methylation regulators and their target genes may provide insight into RA pathogenesis and reveal novel disease regulators and putative drug targets.

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“…FATP5, also called SLC27A5 is mainly expressed in the liver and participates in controlling FFA uptake. As well as carrying out its function as a fatty acid transporter, FATP5 can also activates long-chain fatty acids (LCFAs) through covalent coenzyme A attachment [ 56 ]. It has been reported that deletion or silencing of FATP5 reduces triglyceride levels in the liver and ameliorates diet-induced steatosis in rats [ 57 ].…”

Section: Metabolic-related Genes Influencing Nafldmentioning

confidence: 99%

Exploring the role of genetic variations in NAFLD: implications for disease pathogenesis and precision medicine approaches

Mahmoudi,

Tarzemani,

Aghajanzadeh

et al. 2024

Eur J Med Res

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Non-alcoholic fatty liver disease (NAFLD) is one of the leading causes of chronic liver diseases, affecting more than one-quarter of people worldwide. Hepatic steatosis can progress to more severe forms of NAFLD, including NASH and cirrhosis. It also may develop secondary diseases such as diabetes and cardiovascular disease. Genetic and environmental factors regulate NAFLD incidence and progression, making it a complex disease. The contribution of various environmental risk factors, such as type 2 diabetes, obesity, hyperlipidemia, diet, and sedentary lifestyle, to the exacerbation of liver injury is highly understood. Nevertheless, the underlying mechanisms of genetic variations in the NAFLD occurrence or its deterioration still need to be clarified. Hence, understanding the genetic susceptibility to NAFLD is essential for controlling the course of the disease. The current review discusses genetics’ role in the pathological pathways of NAFLD, including lipid and glucose metabolism, insulin resistance, cellular stresses, and immune responses. Additionally, it explains the role of the genetic components in the induction and progression of NAFLD in lean individuals. Finally, it highlights the utility of genetic knowledge in precision medicine for the early diagnosis and treatment of NAFLD patients.

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Over-Expression and Prognostic Significance of FATP5, as a New Biomarker, in Colorectal Carcinoma

Cited by 4 publications

References 35 publications

Fatty acid transport protein inhibition sensitizes breast and ovarian cancers to oncolytic virus therapy via lipid modulation of the tumor microenvironment

Fatty acid transport protein inhibition sensitizes breast and ovarian cancers to oncolytic virus therapy via lipid modulation of the tumor microenvironment

Diagnostic gene signatures and aberrant pathway activation based on m6A methylation regulators in rheumatoid arthritis

Exploring the role of genetic variations in NAFLD: implications for disease pathogenesis and precision medicine approaches

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