Dietary oleic acid-induced CD36 promotes cervical cancer cell growth and metastasis via up-regulation Src/ERK pathway

Yang, Ping; Su, Chunxiao; Luo, Xianqi; Zeng, Han; Zhao, Lei; Wei, Li; Zhang, Xiaoyu; Varghese, Zac; Moorhead, John F.; Chen, Yaxi; Ruan, Xiong Z.

doi:10.1016/j.canlet.2018.09.006

Cited by 102 publications

(74 citation statements)

References 40 publications

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“…These results suggest that CD36 along with other FA transporters may play a role in the acquired resistance mechanisms of cancer cells. A study previously identified the activation of SRC, and subsequent ERK1/2 activation, through CD36-mediated oleic acid uptake in cervical cancer [167]. Thus, CD36 may promote tumor progression by cross-talking with signaling pathways such as ERK, and therefore targeting CD36 in cancer could be a promising strategy.…”

Section: The Potential Role Of Fatty Acid Metabolism In Mapk Signalinmentioning

confidence: 99%

Targeting MAPK Signaling in Cancer: Mechanisms of Drug Resistance and Sensitivity

Lee

Rauch

Kölch

2020

IJMS

438

298

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Mitogen-activated protein kinase (MAPK) pathways represent ubiquitous signal transduction pathways that regulate all aspects of life and are frequently altered in disease. Here, we focus on the role of MAPK pathways in modulating drug sensitivity and resistance in cancer. We briefly discuss new findings in the extracellular signaling-regulated kinase (ERK) pathway, but mainly focus on the mechanisms how stress activated MAPK pathways, such as p38 MAPK and the Jun N-terminal kinases (JNK), impact the response of cancer cells to chemotherapies and targeted therapies. In this context, we also discuss the role of metabolic and epigenetic aberrations and new therapeutic opportunities arising from these changes.

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Section: The Potential Role Of Fatty Acid Metabolism In Mapk Signalinmentioning

confidence: 99%

Targeting MAPK Signaling in Cancer: Mechanisms of Drug Resistance and Sensitivity

Lee

Rauch

Kölch

2020

IJMS

438

298

View full text Add to dashboard Cite

show abstract

“…Therefore, inhibiting the ERK signaling pathway strengthens the anti-tumor activity of gimatecan in gastric cancer [30]. Activation of ERK signaling results in the promotion of cervical cancer cell growth and metastasis [31]. Interestingly, we found that rL-RVG reduces the phosphorylation levels of MEK/ERK and resulted in a decrease of phosphorylation levels of MLA,α7-nAChR and si-RNA pre-treated groups compared to the ACB pre-treated group.…”

Section: Discussionmentioning

confidence: 65%

Migration of gastric cancer is suppressed by recombinant Newcastle disease virus (rL-RVG) via regulating α7-nicotinic acetylcholine receptors/ERK- EMT

Zhang

Chen

et al. 2019

BMC Cancer

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Background: Nicotinic acetylcholine receptors (nAChRs) have been reported to be overexpressed in malignancies in humans and is associated with tumorigenesis and cell migration. In previous studies of gastric cancer, alpha7 nicotinic acetylcholine receptor (α7-nAChR) overexpression leads to epithelial-mesenchymal transition (EMT) and promotes the migration of gastric cancer cells. Recombinant avirulent LaSota strain of Newcastle disease virus (NDV) expressing the rabies virus glycoprotein (rL-RVG) may promote apoptosis of gastric cancer cells and reduces the migration of lung cancer metastasis. However, whether rL-RVG inhibits migration of gastric cancer cells and what the underlying functional mechanism is remains unknown. Methods: The gastric cancer cell lines BGC and SGC were randomly divided into 3 groups: rL-RVG, NDV and Phosphate Buffered Solution (PBS) control groups. Furthermore,we adopted ACB and MLA,α7nAChR-siRNA for the overexpression and silencing of α7-nAChR.Corynoxenine was used for inhibiting the MEK-ERK pathway. Western blot, Immunofluoresce,cell proliferation assays,cell migration analyses through wound-healing assays and Transwell assays were used to explore the underlying mechanisms. A mouse xenograft model was used to investigate the effects of rL-RVG,NDV on tumor growth. Results: In this study, our findings demonstrate that rL-RVG suppressed the migration of gastric cancer cells and reduced EMT via α7-nAChR in vitro. Furthermore rL-RVG decreased the phosphorylation levels of the MEK/ERK signaling pathway such as down-regulating the expression of P-MEK and PERK. Additionally, rL-RVG also reduced the expression level of mesenchymal markers N-cadherin and Vimentin and enhanced the expression of the epithelial marker E-cadherin. Lastly, rL-RVG inhibited nicotinic acetylcholine receptors (nAChRs) to suppress cell migration and epithelial to mesenchymal transition (EMT) in gastric cell. We also found that rL-RVG suppresses the growth of gastric cancer subcutaneous tumor cells in vivo. Conclusion: rL-RVG inhibits α7-nAChR-MEK/ERK-EMT to suppress migration of gastric cancer cells.

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“…The non-receptor tyrosine kinase Src has been involved in multiple cancer-related process including proliferation and survival through Src-mediated PI3K/AKT/mTOR, MAPK/ ERK and JAK/STAT3 signaling [27][28][29], therefore it has been recently indicated as a promising therapeutic target in the treatment of solid tumors including ESCC [30]. In addition, it has been reported that Src is not only involved in tumor progression but also associated with the resistance to anticancer drugs in traditional and targeted therapies [31].…”

Section: Discussionmentioning

confidence: 99%

Second-generation Src/Abl inhibitor bosutinib effectively induces apoptosis in human esophageal squamous cell carcinoma (ESCC) cells via inhibiting Src/Abl signaling

Ha¹,

Dai²,

Wufuer³

et al. 2020

neo

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Esophageal cancer is a prevalent type of cancer worldwide and is ranked sixth among cancer-associated mortalities. Aberrant activation of the non-receptor tyrosine kinase Src and c-Abl contribute to the progression of ESCC. Thus, targeting these kinases to treat ESCC is a promising strategy. In this paper, we report that the potent dual Src/Abl inhibitor bosutinib exerts anti-tumor effects on ESCC. Bosutinib inhibits ESCC cell proliferation in a dose-dependent manner. Furthermore, bosutinib suppresses the colony formation ability of ESCC cells. Mechanistically, bosutinib effectively inhibits c-Abl and Src and its downstream signaling pathways, PI3K/AKT/mTOR and JAK/STAT3. In addition, bosutinib enhances the cytotoxic effects of doxorubicin on ESCC cells. In summary, our results reveal that Src and Abl are potential therapeutic targets in ESCC and that the novel Src/Abl inhibitor bosutinib alone or in combination with other chemotherapeutic agents may be a viable option for treating ESCC patients.

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Dietary oleic acid-induced CD36 promotes cervical cancer cell growth and metastasis via up-regulation Src/ERK pathway

Cited by 102 publications

References 40 publications

Targeting MAPK Signaling in Cancer: Mechanisms of Drug Resistance and Sensitivity

Targeting MAPK Signaling in Cancer: Mechanisms of Drug Resistance and Sensitivity

Migration of gastric cancer is suppressed by recombinant Newcastle disease virus (rL-RVG) via regulating α7-nicotinic acetylcholine receptors/ERK- EMT

Second-generation Src/Abl inhibitor bosutinib effectively induces apoptosis in human esophageal squamous cell carcinoma (ESCC) cells via inhibiting Src/Abl signaling

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