Brain lipid-binding protein promotes proliferation and modulates cell cycle in C6 rat glioma cells

Han, Xiao; Li, Haoming; Zhang, Ye; Qin, Jianbing; Qiu, Yang; Wang, Lu; Yuan, Mingjie; Xia, Chunlin

doi:10.3892/ijo.2017.4132

Cited by 6 publications

(6 citation statements)

References 54 publications

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“…Western blotting was performed according to previously reported methods ( 24 ). Briefly, following culture for 24 h, a Tissue or Cell Total Protein Extraction kit (Sangon Biotech Co., Ltd.) was used to extract total protein from cells.…”

Section: Methodsmentioning

confidence: 99%

FABP5 regulates the proliferation of clear cell renal cell carcinoma cells via the PI3K/AKT signaling pathway

Wang

Zhang

et al. 2019

Int J Oncol

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Clear cell renal cell carcinoma (ccRCC) has been associated with one of the highest mortality rates among all cancers. Fatty acid binding proteins (FABPs) are 14-15 kDa proteins that are highly abundant in the cytosol of most tissues. FABP5, a member of the FABP family, has been observed to promote tumor cell growth in numerous cancer types. In order to investigate the function of FABP5 in ccRCC cells in the present study, RNA sequencing data from The Cancer Genome Atlas were analyzed to determine the expression levels of FABP5 in ccRCC patient samples. Survival and Cox regression analyses were performed to measure the association between FABP5 expression and clinicopathological features of patients with ccRCC. Subsequent in vitro experiments downregulated or overexpressed FABP5 in Caki-1 and 786O ccRCC cells using lentiviral vectors to evaluate cell proliferation ability, and a xenograft transplantation model was established to examine the effect of FABP5 on tumorigenesis in vivo. The results demonstrated that FABP5 expression was significantly upregulated in samples from patients with ccRCC when compared with normal tissue samples. High FABP5 expression was also significantly correlated with tumor and metastasis classifications and predicted poor survival in patients with ccRCC. In ccRCC cells, silencing of FABP5 significantly inhibited cell proliferation, while overexpression of FABP5 promoted cell proliferation when compared to the respective controls. In addition, treatment with the phosphatidylinositol-4,5-bisphosphate 3-kinase (PI3K)/AKT inhibitor, LY294002, attenuated the pro-proliferative effects of exogenous FABP5 expression in Caki-1 and 786O cells. This indicated that the PI3K/AKT signaling pathway may be partially involved in the FABP5-mediated increase in ccRCC cell proliferation. Furthermore, FABP5 was observed to regulate tumor growth in nude mice in vivo. In conclusion, the results of the present study suggest that FABP5 may exert a pro-proliferative role in ccRCC and may be associated with malignant progression and tumorigenesis.

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Section: Methodsmentioning

confidence: 99%

FABP5 regulates the proliferation of clear cell renal cell carcinoma cells via the PI3K/AKT signaling pathway

Wang

Zhang

et al. 2019

Int J Oncol

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“…The contribution of hypoxia-driven mechanisms to GSC-mediated radioresistance, as discussed by Alhaddad et al [ 40 ] resonates with the findings of Hsieh et al [ 45 ] NADPH oxidase subunit 4, identified as a mediator of cycling hypoxia-promoted radiation resistance in glioblastoma multiforme, underscores the intricate relationship between the tumor microenvironment and resistance mechanisms. The role of hypoxia in shaping the GSC phenotype adds a layer of complexity to the design of targeted therapies, necessitating strategies that account for the dynamic nature of the tumor microenvironment[ 2 , 6 , 46 ].…”

Section: Discussionmentioning

confidence: 99%

Role of glioma stem cells in promoting tumor chemo- and radioresistance: A systematic review of potential targeted treatments

Agosti,

Zeppieri,

Ghidoni

et al. 2024

World J Stem Cells

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BACKGROUND Gliomas pose a significant challenge to effective treatment despite advancements in chemotherapy and radiotherapy. Glioma stem cells (GSCs), a subset within tumors, contribute to resistance, tumor heterogeneity, and plasticity. Recent studies reveal GSCs’ role in therapeutic resistance, driven by DNA repair mechanisms and dynamic transitions between cellular states. Resistance mechanisms can involve different cellular pathways, most of which have been recently reported in the literature. Despite progress, targeted therapeutic approaches lack consensus due to GSCs’ high plasticity. AIM To analyze targeted therapies against GSC-mediated resistance to radio- and chemotherapy in gliomas, focusing on underlying mechanisms. METHODS A systematic search was conducted across major medical databases (PubMed, Embase, and Cochrane Library) up to September 30, 2023. The search strategy utilized relevant Medical Subject Heading terms and keywords related to including “glioma stem cells”, “radiotherapy”, “chemotherapy”, “resistance”, and “targeted therapies”. Studies included in this review were publications focusing on targeted therapies against the molecular mechanism of GSC-mediated resistance to radiotherapy resistance (RTR). RESULTS In a comprehensive review of 66 studies on stem cell therapies for SCI, 452 papers were initially identified, with 203 chosen for full-text analysis. Among them, 201 were deemed eligible after excluding 168 for various reasons. The temporal breakdown of studies illustrates this trend: 2005-2010 (33.3%), 2011-2015 (36.4%), and 2016-2022 (30.3%). Key GSC models, particularly U87 (33.3%), U251 (15.2%), and T98G (15.2%), emerge as significant in research, reflecting their representativeness of glioma characteristics. Pathway analysis indicates a focus on phosphoinositide 3-kinase/protein kinase B/mammalian target of rapamycin (mTOR) (27.3%) and Notch (12.1%) pathways, suggesting their crucial roles in resistance development. Targeted molecules with mTOR (18.2%), CHK1/2 (15.2%), and ATP binding cassette G2 (12.1%) as frequent targets underscore their importance in overcoming GSC-mediated resistance. Various therapeutic agents, notably RNA inhibitor/short hairpin RNA (27.3%), inhibitors (e.g., LY294002, NVP-BEZ235) (24.2%), and monoclonal antibodies (e.g., cetuximab) (9.1%), demonstrate versatility in targeted therapies. among 20 studies (60.6%), the most common effect on the chemotherapy resistance response is a reduction in temozolomide resistance (51.5%), followed by reductions in carmustine resistance (9.1%) and doxorubicin resistance (3.0%), while resistance to RTR is reduced in 42.4% of studies. CONCLUSION GSCs play a complex role in mediating radioresistance and chemoresistance, emphasizing the necessity for precision therapies that consider the heterogeneity within the GSC population and the dynamic tumor microenvironment to enhance outcomes for glioblastoma patients.

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“…Furthermore, BLBP (aka, FABPB or B-FABP) was observed to be localized primarily to astrocytes in the adult brain; thus, it has been used as a marker of mature astrocytes ( Owada et al, 2006 ). Pathologically, BLBP is expressed in glioma cells ( Tian et al, 2018 , Han et al, 2017 ), and intrinsic astrocyte heterogeneity significantly contributes to glioma pathogenesis ( Irvin et al, 2017 ). Moreover, BLBP-expressing astrocytes have also been detected in experimental autoimmune encephalomyelitis ( Kipp et al, 2011 ).…”

Section: Discussionmentioning

confidence: 99%

HOP protein expression in the hippocampal dentate gyrus is acutely downregulated in a status epilepticus mouse model

Alshebib

Hori

Kashiwagi

2021

IBRO Neuroscience Reports

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Status epilepticus (SE) is a neurological emergency, and delayed management can lead to higher morbidity and mortality. It is thought that prolonged seizures stimulate stem cells in the hippocampus and that epileptogenesis may arise from aberrant connections formed by newly born cells, while others have suggested that the acute neuroinflammation and gliosis often seen in epileptic hippocampi contribute to hyperexcitability and epilepsy development. Previous studies have identified the expression of homeodomain-only protein (HOP) in the hippocampal dentate gyrus (HDG) and the heart. HOP was found to be a regulator of cell proliferation and differentiation during heart development, while it maintains the ‘heart conduction system’ in adulthood. However, little is known about HOP function in the adult HDG, particularly in the SE setting. Here, a HOP immunohistochemical profile in an SE mouse model was established. A total of 24 adult mice were analyzed 3–10 days following the SE episode, the ‘acute phase’. Our findings demonstrate a significant downregulation of HOP and BLBP protein expression in the SE group following SE episodes, while HOP/Ki67 coexpression did not remarkably differ. Furthermore, coexpression of HOP/S100β and HOP/Prox1 was not observed, although we noticed insignificant HOP/DCX coexpression level. The findings of this study show no compelling evidence of proliferation, and newly added neurons were not identified during the acute phase following SE, although HOP protein expression was significantly decreased in the HDG. Similar to its counterpart in the adult heart, this suggests that HOP seems to play a key role in regulating signal conduction in adult hippocampus. Moreover, acute changes in HOP expression following SE could be part of an inflammatory response that could subsequently influence epileptogenicity.

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Brain lipid-binding protein promotes proliferation and modulates cell cycle in C6 rat glioma cells

Cited by 6 publications

References 54 publications

FABP5 regulates the proliferation of clear cell renal cell carcinoma cells via the PI3K/AKT signaling pathway

FABP5 regulates the proliferation of clear cell renal cell carcinoma cells via the PI3K/AKT signaling pathway

Role of glioma stem cells in promoting tumor chemo- and radioresistance: A systematic review of potential targeted treatments

HOP protein expression in the hippocampal dentate gyrus is acutely downregulated in a status epilepticus mouse model

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