Leupaxin Promotes Bladder Cancer Proliferation, Metastasis, and Angiogenesis Through the PI3K/AKT Pathway

Hou, Teng; Zhou, Lijie; Wang, Longwang; Kazobinka, Gallina; Chen, Yumao; Zhang, Xiaoping; Chen, Zhaohui

doi:10.1159/000491536

Cited by 26 publications

(20 citation statements)

References 23 publications

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“…PI3K/Akt signaling pathway can act as an inducer of metastasis in several malignancies including BC cells [ 100 , 101 , 102 ]. Anti-tumor agents such as leupaxin can suppress invasion of BC cells via PI3K/Akt downregulation [ 103 ]. miRNA-328-3p is considered as an onco-suppressor factor in BC cells.…”

Section: Micrornas Inhibit Emt In Bladder Cancer Cellsmentioning

confidence: 99%

Role of microRNA/Epithelial-to-Mesenchymal Transition Axis in the Metastasis of Bladder Cancer

et al. 2020

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Bladder cancer (BC) is the 11th most common diagnosed cancer, and a number of factors including environmental and genetic ones participate in BC development. Metastasis of BC cells into neighboring and distant tissues significantly reduces overall survival of patients with this life-threatening disorder. Recently, studies have focused on revealing molecular pathways involved in metastasis of BC cells, and in this review, we focus on microRNAs (miRNAs) and their regulatory effect on epithelial-to-mesenchymal transition (EMT) mechanisms that can regulate metastasis. EMT is a vital process for migration of BC cells, and inhibition of this mechanism restricts invasion of BC cells. MiRNAs are endogenous non-coding RNAs with 19–24 nucleotides capable of regulating different cellular events, and EMT is one of them. In BC cells, miRNAs are able to both induce and/or inhibit EMT. For regulation of EMT, miRNAs affect different molecular pathways such as transforming growth factor-beta (TGF-β), Snail, Slug, ZEB1/2, CD44, NSBP1, which are, discussed in detail this review. Besides, miRNA/EMT axis can also be regulated by upstream mediators such as lncRNAs, circRNAs and targeted by diverse anti-tumor agents. These topics are also discussed here to reveal diverse molecular pathways involved in migration of BC cells and strategies to target them to develop effective therapeutics.

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Section: Micrornas Inhibit Emt In Bladder Cancer Cellsmentioning

confidence: 99%

Role of microRNA/Epithelial-to-Mesenchymal Transition Axis in the Metastasis of Bladder Cancer

et al. 2020

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“…Numerous studies have confirmed that the phosphatidylinositol-3 kinase (PI3K)/Akt (protein kinase B)/mammalian target of rapamycin (mTOR) pathway plays an important role in cell proliferation, metastasis and angiogenesis in bladder cancer [8,9]. Moreover, studies have demonstrated that blocking the PI3K/Akt/mTOR pathway can be a potential therapeutic strategy [10].…”

Section: Introductionmentioning

confidence: 99%

Cryptotanshinone Inhibites Bladder Cancer Cell Proliferation and Promotes Apoptosis via the PTEN/PI3K/AKT Pathway

Liu¹,

Lin²,

Chen³

et al. 2020

J. Cancer

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Cryptotanshinone (CTT), extracted from the root of Salvia miltiorrhiza Bunge (Danshen), exhibits activities against a variety of human cancers in vitro and in vivo. The purpose of this study was to investigate the potential inhibitory effect of CTT on bladder cancer. In this study, we found that CTT inhibited bladder cancer cell proliferation, migration, and invasion and promoted apoptosis. In addition, CTT modulated the expression of proteins via the PI3K/AKT pathway, and the inhibition of PI3K/AKT signalling was due to induction of PTEN expression. Taken together, the results of the present study demonstrated the anticancer effect of CTT on bladder cancer cells, which might be associated with the downregulation of PI3K/AKT/mTOR and NF-κB signalling pathway proteins, and this inhibition was mediated by the induction of PTEN.

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“…The phosphatidylinositol-4,5-bisphosphate 3-kinase (PI3K)/AKT signaling pathway is involved in numerous diverse cellular functions, including cell proliferation (6), differentiation (7), angiogenesis (8) and autophagy (9). The PI3K/AKT signaling pathway also affects epithelial-mesenchymal transition (EMT) via multiple regulatory mechanisms, which influences tumor aggressiveness (10).…”

Section: Introductionmentioning

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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Leupaxin Promotes Bladder Cancer Proliferation, Metastasis, and Angiogenesis Through the PI3K/AKT Pathway

Cited by 26 publications

References 23 publications

Role of microRNA/Epithelial-to-Mesenchymal Transition Axis in the Metastasis of Bladder Cancer

Role of microRNA/Epithelial-to-Mesenchymal Transition Axis in the Metastasis of Bladder Cancer

Cryptotanshinone Inhibites Bladder Cancer Cell Proliferation and Promotes Apoptosis via the PTEN/PI3K/AKT Pathway

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

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