Lectin-like oxidized low-density lipoprotein receptor-1 facilitates metastasis of gastric cancer through driving epithelial-mesenchymal transition and PI3K/Akt/GSK3β activation

Li, Can; Zhang, Jie; Wu, Hao; Li, Lili; Yang, Caiting; Song, Shushu; Peng, Peike; Shao, Miaomiao; Zhang, Mingming; Zhao, Junjie; Zhao, Ran; Wu, Weicheng; Ruan, Yuanyuan; Wang, Lan; Gu, Jianxin

doi:10.1038/srep45275

Cited by 41 publications

(25 citation statements)

References 47 publications

(53 reference statements)

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“…Each year, about 700,000 deaths were caused by GC, alarming the world of its diagnosis and treatment (Ferlay et al, ). Previous studies have certified that PI3K is an oncogene and P53 is a tumor suppressor gene in GC (Du, Liu, Wang, & Wang, ; Li et al, ). The present study showed that curcumin, a natural phytochemical, could inhibit PI3K pathway and activate P53 pathway in GC cells, thereby inducing apoptosis and autophagy.…”

Section: Discussionmentioning

confidence: 96%

Curcumin regulates proliferation, autophagy, and apoptosis in gastric cancer cells by affecting PI3K and P53 signaling

Wang

Yang

et al. 2018

Journal Cellular Physiology

141

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In this study, we aimed to investigate the effects of curcumin on cell activities of gastric cancer (GC), and the connection between curcumin and P53, as well as, PI3K signaling. This study was conducted with two cell lines SGC-7901 and BGC-823, both were exposed to curcumin at the concentrations of 0, 10, 20, and 40 μm. MTT assay, flow cytometry (FCM) assay, transmission electron microscopy (TEM) were used to study the underlying mechanisms of curcumin in respective of proliferation, apoptosis, and autophagy. Western blot assay was also employed to detect impacts of curcumin on tophosphatidylinositol-3 kinase (PI3K) and P53 signaling pathways-related proteins. MTT assay displayed that curcumin inhibited GC cell proliferation. FCM results indicated that curcumin induced the apoptosis of GC cells. TEM revealed that curcumin induced autophagy in GC cells. Western blot results showed that curcumin activated P53 signaling pathway and inhibited PI3K signaling pathway. Curcumin may inhibit proliferation and induce the autophagy and apoptosis in GC cells. Additionally, curcumin activated the P53 signaling pathway by up-regulating P53 and P21, which also inhibited PI3K pathway through down-regulating PI3K, p-Akt, and p-mTOR.

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Section: Discussionmentioning

confidence: 96%

Curcumin regulates proliferation, autophagy, and apoptosis in gastric cancer cells by affecting PI3K and P53 signaling

Wang

Yang

et al. 2018

Journal Cellular Physiology

141

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“…Metastasis is a high potential risk and the predominant cause of recurrence and mortality among patients with GC, and a number of cell biological activities are controlled in this multistep process, including adhesion, migration, invasion and angiogenesis (1). Lectin-like oxidized low-density lipoprotein receptor-1 was overexpressed in GC cells and increased the migratory and invasive ability by enhancing EMT, and activating the PI3K/Akt/glycogen synthase kinase 3β (GSK3β) pathway (53). Vascular endothelial growth factor-A (VEGF-A) was suggested to promote angiogenesis by activating the downstream Akt/mTOR cascade in GC (24).…”

Section: Direct Sequencingmentioning

confidence: 99%

MicroRNAs and the PTEN/PI3K/Akt pathway in gastric cancer (Review)

Zhu

Xiong

et al. 2019

Oncol Rep

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Gastric carcinogenesis arises from complicated interactions among host, environmental and bacterial factors, which cause genetic and epigenetic dysregulation of oncogenic and tumor-suppressive genes. MicroRNAs (miRNAs), a class of small non-coding RNAs that post-transcriptionally regulate ~30% human genes, may serve as oncogenes or tumor-suppressors in malignancies, including gastric cancer (GC). Although miRNA dysregulation commonly exists in GC, exact roles miRNAs serve in the pathogenesis and promotion of this tumor remain undetermined. Recently, results of previous studies regarding mechanisms underlying miRNAs generally converged on pathways critical in cellular processes, including cell proliferation, apoptosis and invasion, among which phosphatase and tensin homolog (PTEN)/phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt) signaling is a fundamental one, with frequent oncogenic alterations in GC. Therefore, in the present review, the disorder and function of miRNAs and PTEN/PI3K/Akt signaling in GC are discussed. Additionally, how miRNAs transduce their effects by regulating this pathway, particularly in GC stem cells and the tumor microenvironment, and two novel hypotheses significant in carcinogenesis, tumor progression and recurrence, are discussed. Furthermore, the roles of miRNAs and the PTEN/PI3K/Akt pathway in target therapies against this lethal disease are outlined.

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“…In line with these findings, targeting influenza histocompatibility antigen-1 to LOX-1 elicits antigen-specific protective antibody response to virus in macaques suggesting a good candidate for vaccine development ( 39 ). Besides, several studies have reported a high expression of LOX-1 in various tumors including gastric ( 40 ), colorectal ( 41 ), and prostate ( 42 ) cancers, which correlates with a poor prognosis in patients ( 40 ). Functionally, LOX-1 was shown to promote tumor angiogenesis ( 42 ), metastasis ( 43 ), and the migration and invasion of gastric cancer cells by notably driving epithelial–mesenchymal transition ( 40 ).…”

Section: “(Dectin-1)” Familymentioning

confidence: 99%

“…Besides, several studies have reported a high expression of LOX-1 in various tumors including gastric ( 40 ), colorectal ( 41 ), and prostate ( 42 ) cancers, which correlates with a poor prognosis in patients ( 40 ). Functionally, LOX-1 was shown to promote tumor angiogenesis ( 42 ), metastasis ( 43 ), and the migration and invasion of gastric cancer cells by notably driving epithelial–mesenchymal transition ( 40 ). Interestingly, LOX-1 was recently identified to be particularly expressed by potent polymorphonuclear myeloid-derived suppressor cells from blood and tumor of patients with non-small cell lung or head neck cancer and to be associated with worse survival ( 44 ).…”

Section: “(Dectin-1)” Familymentioning

confidence: 99%

C-Type Lectin-Like Receptors As Emerging Orchestrators of Sterile Inflammation Represent Potential Therapeutic Targets

Chiffoleau

2018

Front. Immunol.

117

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Over the last decade, C-type lectin-like receptors (CTLRs), expressed mostly by myeloid cells, have gained increasing attention for their role in the fine tuning of both innate and adaptive immunity. Not only CTLRs recognize pathogen-derived ligands to protect against infection but also endogenous ligands such as self-carbohydrates, proteins, or lipids to control homeostasis and tissue injury. Interestingly, CTLRs act as antigen-uptake receptors via their carbohydrate-recognition domain for internalization and subsequent presentation to T-cells. Furthermore, CTLRs signal through a complex intracellular network leading to the secretion of a particular set of cytokines that differently polarizes downstream effector T-cell responses according to the ligand and pattern recognition receptor co-engagement. Thus, by orchestrating the balance between inflammatory and resolution pathways, CTLRs are now considered as driving players of sterile inflammation whose dysregulation leads to the development of various pathologies such as autoimmune diseases, allergy, or cancer. For examples, the macrophage-inducible C-type lectin (MINCLE), by sensing glycolipids released during cell-damage, promotes skin allergy and the pathogenesis of experimental autoimmune uveoretinitis. Besides, recent studies described that tumors use physiological process of the CTLRs’ dendritic cell-associated C-type lectin-1 (DECTIN-1) and MINCLE to locally suppress myeloid cell activation and promote immune evasion. Therefore, we aim here to overview the current knowledge of the pivotal role of CTLRs in sterile inflammation with special attention given to the “Dectin-1” and “Dectin-2” families. Moreover, we will discuss the potential of these receptors as promising therapeutic targets to treat a wide range of acute and chronic diseases.

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Lectin-like oxidized low-density lipoprotein receptor-1 facilitates metastasis of gastric cancer through driving epithelial-mesenchymal transition and PI3K/Akt/GSK3β activation

Cited by 41 publications

References 47 publications

Curcumin regulates proliferation, autophagy, and apoptosis in gastric cancer cells by affecting PI3K and P53 signaling

Curcumin regulates proliferation, autophagy, and apoptosis in gastric cancer cells by affecting PI3K and P53 signaling

MicroRNAs and the PTEN/PI3K/Akt pathway in gastric cancer (Review)

C-Type Lectin-Like Receptors As Emerging Orchestrators of Sterile Inflammation Represent Potential Therapeutic Targets

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