Hepatocellular carcinoma cells cause different responses in expressions of cancer‐promoting genes in different cancer‐associated fibroblasts

Lin, Zu‐Yau; Chuang, Wan‐Long

doi:10.1016/j.kjms.2012.08.012

Cited by 31 publications

(19 citation statements)

References 40 publications

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“…Apelin is a regulatory peptide identified as an endogenous ligand of the apelin receptor APJ . Apelin and its receptor have been reported to stimulate endothelial growth in different in vitro and in vivo experimental systems, and some recent studies have shown that apelin expression is detected at a high levels in breast cancer, oral squamous cell carcinoma, and liver cancer . In the present study, we found that apelin is not only significantly upregulated in lung adenocarcinoma tissues compared to adjacent healthy lung tissues but also positively correlated with poor prognosis of patients with lung adenocarcinoma.…”

Section: Discussionsupporting

confidence: 66%

“…It has been reported that apelin, as a novel angiogenic factor, is involved in the regulation of cardiovascular function and promotion of angiogenesis, lymphangiogenesis, and tumor growth in vivo, and the angiogenic potential of apelin is similar to that of VEGF . Previous studies demonstrated that apelin has aberrantly high expression and high apelin protein levels are associated with cell proliferation, angiogenesis, and prognosis in various cancers, including breast, lung, oral, liver, and colon cancers . However, the molecular mechanisms involved in the upstream regulation of apelin expression in lung adenocarcinoma remain unknown.…”

Section: Introductionmentioning

confidence: 99%

“…6,7 Previous studies demonstrated that apelin has aberrantly high expression and high apelin protein levels are associated with cell proliferation, angiogenesis, and prognosis in various cancers, including breast, lung, oral, liver, and colon cancers. [8][9][10][11][12] However, the molecular mechanisms involved in the upstream regulation of apelin expression in lung adenocarcinoma remain unknown.…”

Section: Introductionmentioning

confidence: 99%

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MicroRNA‐195 suppresses the progression of lung adenocarcinoma by directly targeting apelin

Zhou

Zhao

et al. 2019

Thoracic Cancer

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Background Apelin plays an important role in many types of tumors. We aimed to identify the effects of miR‐195 on inhibiting apelin and clarify the regulating mechanism of miR‐195‐apelin in lung adenocarcinoma cells. Methods We detected the expression levels of apelin and miR‐195 in lung adenocarcinoma tissues and lung cancer cell lines using Western blotting and quantitative reverse transcription PCR assay, respectively. Luciferase reporter assay was used to confirm the target gene of miR‐195. The effects of miR‐195 and apelin on the proliferation and cell cycle of lung adenocarcinoma cells were assessed by methyl thiazolyl tetrazolium and colony formation assays, and flow cytometry. Wound‐healing and transwell invasion experiments were employed to examine cellular migration and invasion. A tumor xenograft model was then used to investigate the role of miR‐195 on tumor growth in vivo. Results The expression level of apelin and miR‐195 showed an inverse correlation in lung adenocarcinoma tissues and cell lines. Luciferase reporter assay suggested that miR‐195 directly targets apelin messenger RNA. Overexpression of miR‐195 significantly inhibited the proliferation, migration, and invasion of lung adenocarcinoma cells in vitro and suppressed tumor growth in vivo. Further analysis revealed that apelin is one of the functional target genes of miR‐195, and the overexpression of apelin efficiently inhibits the promotion of cell proliferation and invasion mediated by miR‐195 mimics in lung adenocarcinoma cells. Conclusions Our data constitute evidence that miR‐195 inhibits lung adenocarcinoma cell proliferation and invasion though targeting apelin and provides novel insight into the mechanism underlying the development of lung adenocarcinoma.

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Section: Discussionsupporting

confidence: 66%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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MicroRNA‐195 suppresses the progression of lung adenocarcinoma by directly targeting apelin

Zhou

Zhao

et al. 2019

Thoracic Cancer

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“…[18][19][20] Also, cancer cells could maintain the CAF phenotype and promote functions such as proliferation, migration, invasion, or angiogenesis. 21 In our study, after stimulation with cancer cell-cultured medium, the migration and invasion-promoting function of CAF clearly increased.…”

Section: Discussionsupporting

confidence: 54%

Nab‐paclitaxel interrupts cancer‐stromal interaction through C‐X‐C motif chemokine 10‐mediated interleukin‐6 downregulation in vitro

et al. 2018

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Cancer‐associated fibroblasts (CAF), derived from stroma of cancer tissues, interact with cancer cells and play an important role in cancer initiation, growth, and metastasis. Nab‐paclitaxel (nab‐PTX) is a 130 nm albumin‐binding paclitaxel and recommended for many types of cancer chemotherapy. The nab‐PTX stromal‐disrupting effect during pancreatic cancer treatment has been reported. The aim of the present study was to determine the role of nab‐PTX in cancer cells and CAF interaction. Cancer cells (MIA PaCa‐2 and Panc‐1) were cocultured with CAF or treated with CAF conditioned medium, after which their migration and invasion ability, epithelial‐mesenchymal transition (EMT)‐related marker expression and C‐X‐C motif chemokine 10 (CXCL10) expression and secretion were detected. Nab‐PTX treatment was carried out during the coculture system or during preparation of CAF conditioned medium. Then cancer cell migration and invasion ability, EMT‐related marker expression, CXCL10 expression and secretion, and interleukin‐6 (IL‐6) expression and secretion by CAF were checked After coculture with CAF, migration and invasion ability of cancer cells increased. CAF also downregulated E‐cadherin and upregulated N‐cadherin and vimentin expression in cancer cells. During coculture or stimulation with cancer cell‐cultured medium, CAF significantly increased IL‐6 expression and secretion. However, nab‐PTX in the coculture system canceled CAF‐induced migration and invasion promotion and EMT‐related gene changes. Moreover, nab‐PTX increased CXCL10 expression of cancer cells which blocked CAF IL‐6 expression and secretion. Nab‐PTX treatment could increase CXCL10 expression of cancer cells which blocks CAF cancer cell migration and invasion‐promoting effect by inhibiting IL‐6 expression.

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“…Chuang et al . demonstrated [18, 19] that co-culture of HCCs and CAFs in vitro can enhance proliferation, migration, and invasion of HCC by changing of gene expression in HCC cell lines. H-CAFs can specifically up-regulate CCL2, CCL26, IL6, and LOXL2 genes which are related to proliferation, migration, invasion and angiogenesis in HCC cells.…”

Section: Influence Of the Tme Componentsmentioning

confidence: 99%

Roles of Tumor Microenvironment in Hepatocelluar Carcinoma

Seo

2015

CCTR

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Hepatocellular carcinoma (HCC) is one of the most malignant human cancers, with a high mortality rate worldwide despite its early diagnosis in patients and improvement in therapeutic technology. Most cases of liver cancer show a strong resistance to anticancer therapy. Moreover, liver cancer patients generally have poor tolerance to chemotherapy due to liver dysfunction. In these situations, liver-targeting drugs with fewer side effects and a high efficacy are urgently needed during drug discovery for liver cancer. Researchers have aimed to derive target genes and drug candidates for HCC; however, the development of targeted drugs has not yet improved the outcome significantly.Recently, the role of the tumor microenvironment (TME) in HCC has been probed to combat this deadly disease. A deeper knowledge of the crosstalk between tumor cells and their TME is needed to fully understand tumor development, progression and chemo-resistance in HCC because this cancer develops from chronically damaged tissue that contains large amounts of inflammation and fibrosis.In this review, we summarize how distinct stromal cells of TME are involved in tumorigenesis and chemo-resistance in HCC and the significant challenge to recapitulate tumor complexity and heterogeneity enhancement.

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Hepatocellular carcinoma cells cause different responses in expressions of cancer‐promoting genes in different cancer‐associated fibroblasts

Cited by 31 publications

References 40 publications

MicroRNA‐195 suppresses the progression of lung adenocarcinoma by directly targeting apelin

MicroRNA‐195 suppresses the progression of lung adenocarcinoma by directly targeting apelin

Nab‐paclitaxel interrupts cancer‐stromal interaction through C‐X‐C motif chemokine 10‐mediated interleukin‐6 downregulation in vitro

Roles of Tumor Microenvironment in Hepatocelluar Carcinoma

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