Enhancement of invasion of hepatocellular carcinoma cells through lysophosphatidic acid receptor

Lou, Lianqing; Chen, Yong Xin; Jin, Lingzhen; Li, Xiaofei; Tao, Xingfei; Zhu, Jinhong; Chen, Xiangyi; Wu, Shuang; Ye, Weiwei; He, Jinke; Ding, Guoqiang

doi:10.1177/0300060512474124

Cited by 11 publications

(7 citation statements)

References 31 publications

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“…Association of LPA-mediated signaling with tumor progression in carcinomas other than urothelial carcinoma has been reported. In hepatocellular carcinoma, LPA stimulates cancer cell invasion in a LPA-receptor dependent manner [19]. In prostate carcinoma, increased LPA-dependent RHO signaling enhances tumor invasion [20].…”

Section: Resultsmentioning

confidence: 99%

Expression and Role of GPR87 in Urothelial Carcinoma of the Bladder

Okazoe

Zhang

Liu

et al. 2013

IJMS

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The orphan GPR87 has recently been matched with its ligand LPA, which is a lipid mediator with multiple physiological functions, including cancer cell proliferation. This study aimed to clarify the role of GPR87 in urothelial carcinoma of the bladder. GPR87 expression was assessed in seven human bladder cancer cell lines. A replication-deficient recombinant adenoviral vector expressing shRNA targeting GPR87 (Ad-shGPR87), was constructed. Gene silencing was carried out using Ad-shGPR87. Immunohistochemical analysis was performed for transurethral resection of bladder tumor samples from 71 patients with non-muscle-invasive bladder cancer. We observed GPR87 expression in five of the seven cell lines, and silencing GPR87 gene expression significantly reduced cell viability. GPR87 expression was positive in 38 (54%) of 71 tumors. Ki-67 index was associated with positive GPR87 staining status (p < 0.0001). Patients with GPR87-positive tumors had shorter intravesical recurrence-free survival than those with GPR87-negative tumors (p = 0.010). Multivariate analysis revealed that GPR87 staining status was an independent prognostic parameter for intravesical recurrence (p = 0.041). Progression from non-muscle-invasive to muscle-invasive tumor was more frequently observed in patients with GPR87-positive tumors, although this trend did not reach statistical significance (p = 0.056). These results warrant further prospective studies to clarify the role of GPR87 expression in intravesical recurrence and progression in bladder cancer.

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Section: Resultsmentioning

confidence: 99%

Expression and Role of GPR87 in Urothelial Carcinoma of the Bladder

Okazoe

Zhang

Liu

et al. 2013

IJMS

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“…Ki16425 was reportedly able to significantly reduce pancreatic cancer development [105] and reduce hepatocarcinoma tumor cell invasion and lung metastases [77]. Furthermore, Ki16452 can significantly reduce LPA-related HCC cell invasion [106]. Moreover, silencing of LPA1 or treatment with Ki1625 was demonstrated to lead to the inhibition of sphere-forming ability, tumorigenicity, and drug resistance in ovarian CSC [61].…”

Section: Development Of Inhibitors Against the Atx-lpa Signaling Axismentioning

confidence: 99%

Role of autotaxin in cancer stem cells

Lee

Suh

Lee

et al. 2018

Cancer Metastasis Rev

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Stem cells are a rare subpopulation defined by the potential to self-renew and differentiate into specific cell types. A population of stem-like cells has been reported to possess the ability of self-renewal, invasion, metastasis, and engraftment of distant tissues. This unique cell subpopulation has been designated as cancer stem cells (CSC). CSC were first identified in leukemia, and the contributions of CSC to cancer progression have been reported in many different types of cancers. The cancer stem cell hypothesis attempts to explain tumor cell heterogeneity based on the existence of stem cell-like cells within solid tumors. The elimination of CSC is challenging for most human cancer types due to their heightened genetic instability and increased drug resistance. To combat these inherent abilities of CSC, multi-pronged strategies aimed at multiple aspects of CSC biology are increasingly being recognized as essential for a cure. One of the most challenging aspects of cancer biology is overcoming the chemotherapeutic resistance in CSC. Here, we provide an overview of autotaxin (ATX), lysophosphatidic acid (LPA), and their signaling pathways in CSC. Increasing evidence supports the role of ATX and LPA in cancer progression, metastasis, and therapeutic resistance. Several studies have demonstrated the ATX-LPA axis signaling in different cancers. This lipid mediator regulatory system is a novel potential therapeutic target in CSC. In this review, we summarize the evidence linking ATX-LPA signaling to CSC and its impact on cancer progression and metastasis. We also provide evidence for the efficacy of cancer therapy involving the pharmacological inhibition of this signaling pathway.

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“…Defining the mechanisms regulating HCC invasion may identify novel elements, which may be exploited therapeutically to reduce metastasis and improve patient survival. The process of metastasis involves several steps, including the detachment of cancer cells from the primary tumour, followed by the migration, adhesion and invasion of cancer cells into blood or lymphatic vessels; cancer cells then undergo extravasation and subsequently interact with target tissues, where they form metastastic foci in distant organs (41). The destruction of the extracellular matrix (ECM) by enzymes is an essential initial step in the processes of tumor cell invasion and metastasis, and several studies have reported that, among the enzymes responsible for ECM degradation, MMPs are have a critical role (42,43).…”

Section: Mmp-9 Is a Direct Target Gene Of Mir-133a In Hccmentioning

confidence: 99%

MicroRNA-133a inhibits cell proliferation, colony formation ability, migration and invasion by targeting matrix metallopeptidase 9 in hepatocellular carcinoma

Chen

Zhao

et al. 2015

Molecular Medicine Reports

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Abstract. is downregulated in various types of human malignancy, including hepatocellular carcinoma (HCC), renal cell carcinoma, esophageal squamous cell carcinoma, bladder cancer, ileal carcinoid and rhabdomyosarcoma. The aim of the present study was to examine the effects of miR-133a on HCC cell proliferation, colony formation, migration and invasion. miR-133a was transfected into the HCC HepG2 and SMMC-7721 cell lines and the expression levels of miR-133a were determined; in addition, cell viability assays, colony formation assays, cell migration assays, cell invasion assays, western blot analyses and luciferase assays were performed in the HCC cell lines. The results demonstrated that miR-133a significantly inhibited cell proliferation, colony formation, migration and invasion in HepG2 and SMMC-7721 cells. To the best of our knowledge, the present study also provided the first evidence that miR-133a directly downregulated the expression of matrix metallopeptidase 9 (MMP-9) in the HCC cells. In conclusion, the results of the present study indicated that miR-133a may have suppressed cell proliferation, colony formation, migration and invasion via the downregulation of MMP-9 in HCC cell lines. Therefore, MMP-9 may be used for the development of novel molecular markers and therapeutic approaches to inhibit hepatocellular carcinoma metastasis.

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Enhancement of invasion of hepatocellular carcinoma cells through lysophosphatidic acid receptor

Cited by 11 publications

References 31 publications

Expression and Role of GPR87 in Urothelial Carcinoma of the Bladder

Expression and Role of GPR87 in Urothelial Carcinoma of the Bladder

Role of autotaxin in cancer stem cells

MicroRNA-133a inhibits cell proliferation, colony formation ability, migration and invasion by targeting matrix metallopeptidase 9 in hepatocellular carcinoma

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