Elevated expression of growth-regulated oncogene-alpha in tumor and stromal cells predicts unfavorable prognosis in pancreatic cancer

Lian, Shuijin; Zhai, Xiaolu; Wang, Xudong; Zhu, Huijun; Zhang, Shu; Wang, Wei; Wang, Zhiwei; Huang, Jianfei

doi:10.1097/md.0000000000004328

Cited by 24 publications

(22 citation statements)

References 37 publications

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“…Certain studies have suggested that patients with pancreatic, gastric or hepatocellular cancer exhibit increased levels of CXCL1 in cancer tissues (38-40). By contrast, other studies have demonstrated that CXCL1 mRNA expression levels in hepatic tumors were similar between cancerous and non-cancerous tissues (41).…”

Section: Discussionmentioning

confidence: 99%

CXCL1 stimulates migration and invasion in ER‑negative breast cancer cells via activation of the ERK/MMP2/9 signaling axis

Yang

Chen

et al. 2019

Int J Oncol

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Chemokine (C-X-C motif) ligand 1 (CXCL1), a member of the CXC chemokine family, has been reported to be a critical factor in inflammatory diseases and tumor progression; however, its functions and molecular mechanisms in estrogen receptor α (ER)-negative breast cancer (BC) remain largely unknown. The present study demonstrated that CXCL1 was upregulated in ER-negative BC tissues and cell lines compared with ER-positive tissues and cell lines. Treatment with recombinant human CXCL1 protein promoted ER-negative BC cell migration and invasion in a dose-dependent manner, and stimulated the activation of phosphorylated (p)- extracellular signal-regulated kinase (ERK)1/2, but not p-STAT3 or p-AKT. Conversely, knockdown of CXCL1 in BC cells attenuated these effects. Additionally, CXCL1 increased the expression of matrix metalloproteinase (MMP)2/9 via the ERK1/2 pathway. Inhibition of MEK1/2 by its antagonist U0126 reversed the effects of CXCL1 on MMP2/9 expression. Furthermore, immunohistochemical analysis revealed a strong positive association between CXCL1 and p-ERK1/2 expression levels in BC tissues. In conclusion, the present study demonstrated that CXCL1 is highly expressed in ER-negative BC, and stimulates BC cell migration and invasion via the ERK/MMP2/9 pathway. Therefore, CXCL1 may serve as a potential therapeutic target in ER-negative BC.

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Section: Discussionmentioning

confidence: 99%

CXCL1 stimulates migration and invasion in ER‑negative breast cancer cells via activation of the ERK/MMP2/9 signaling axis

Yang

Chen

et al. 2019

Int J Oncol

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“…A clinical significance to growth-regulated oncogene- α has been assigned by Lian and collaborators. In a recent study, they observed higher level of this chemokine in pancreatic cancer tissues as compared to normal ones, and the expression was correlated with TNM stage and metastases localization, thus leading to significant poor survival of patients [105].…”

Section: The Role Of Cytokines In Colorectal and Pancreatic Cancermentioning

confidence: 99%

Advances in Tumor-Stroma Interactions: Emerging Role of Cytokine Network in Colorectal and Pancreatic Cancer

Bazzichetto

Cognetti

Falcone

et al. 2019

Journal of Oncology

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Cytokines are a family of soluble factors (Growth Factors (GFs), chemokines, angiogenic factors, and interferons), which regulate a wide range of mechanisms in both physiological and pathological conditions, such as tumor cell growth and progression, angiogenesis, and metastasis. In recent years, the growing interest in developing new cancer targeted therapies has been accompanied by the effort to characterize Tumor Microenvironment (TME) and Tumor-Stroma Interactions (TSI). The connection between tumor and stroma is now well established and, in the last decade, evidence from genetic, pharmacological, and epidemiological data supported the importance of microenvironment in tumor progression. However, several of the mechanisms behind TSI and their implication in tumor progression remain still unclear and it is crucial to establish their potential in determining pharmacological response. Many studies have demonstrated that cytokines network can profoundly affect TME, thus displaying potential therapeutic efficacy in both preclinical and clinical models. The goal of this review is to give an overview of the most relevant cytokines involved in colorectal and pancreatic cancer progression and their implication in drug response.

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“…Additionally, GRO has an important role in wound healing by modulating cell migration and angiogenesis as well. In particular, GRO-α seems to promote cancer proliferation, angiogenesis and metastasis (33,34). The dot blot assay revealed that wound fluid (WF) contains several factors that have mitogenic effects on cancer cells.…”

Section: Discussionmentioning

confidence: 99%

Wound fluid enhances cancer cell proliferation via activation of STAT3 signal pathway in vitro

et al. 2019

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Wound healing begins immediately after surgery with a modification of the microenvironment via a well-orchestrated interaction between cells, cytokines and growth factors. Some of these growth factors and cytokines have mitogenic effects on cancer cells, which may lead to enhanced cancer cell proliferation and early metastatic events. The present study aimed to investigate the effects of wound fluid (WF) on the head and neck squamous carcinoma cell lines FaDu and HLaC78 in vitro. WF was harvested from 7 patients who had undergone a planned neck dissection. The presence of cytokines and growth factors was evaluated with the dot blot assay. Proliferation and cell viability were investigated via MTT assay and Ki-67 staining. Cell invasion was measured via tree-dimensional invasion assay. Western blotting was used to investigate STAT 3 activation. WF contained several cytokines and growth factors responsible for pro-and anti-inflammation, chemotaxis, proliferation and angiogenesis. The proliferation effect of WF on FaDu and HLaC78 was concentration dependent. Media with 40% WF resulted in the highest proliferation effect. FaDu and HLaC78 exhibited enhanced motility after cultivation with 40% WF compared with cultivation with expansion medium. Cultivating cancer cells with WF had no advantageous effect on cell viability after the paclitaxel treatment. Western blot analysis revealed enhanced activation of the STAT3 signaling pathway by WF in both FaDu and HLaC78. In conclusion, surgery leads to excessive release of mitogenic factors. The contact of non-resected cancer cells and these factors may have a negative impact on patient outcome. Future investigations should specifically focus on the inhibition of mitogenic factors following cancer surgery in order to prevent early metastasis and cancer recurrence.

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Elevated expression of growth-regulated oncogene-alpha in tumor and stromal cells predicts unfavorable prognosis in pancreatic cancer

Cited by 24 publications

References 37 publications

CXCL1 stimulates migration and invasion in ER‑negative breast cancer cells via activation of the ERK/MMP2/9 signaling axis

CXCL1 stimulates migration and invasion in ER‑negative breast cancer cells via activation of the ERK/MMP2/9 signaling axis

Advances in Tumor-Stroma Interactions: Emerging Role of Cytokine Network in Colorectal and Pancreatic Cancer

Wound fluid enhances cancer cell proliferation via activation of STAT3 signal pathway in vitro

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