Platelet-derived growth factor-B signalling might promote epithelial-mesenchymal transition in gastric carcinoma cells through activation of the MAPK/ERK pathway

Yin, Jiangyan; Guo, Yi; Li, Zhongfu

doi:10.5114/wo.2021.103938

Cited by 3 publications

(2 citation statements)

References 40 publications

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“…Our RNA-seq data revealed that KLF7 is linked with several cancer signaling pathways, such as PI3K/AKT, JAK/STAT3, and MAPK/ERK in COAD. The PI3K/AKT, JAK/STAT3, and MAPK/ERK signaling pathways are frequently activated in COAD and involved in metastasis [40][41][42] .The PDGF signaling activates the JAK/ STAT3, PI3K/AKT, and MAPK/ERK pathways [43][44][45] . Our RNA-seq data indicated that PDGFB was a differentially expressed gene commonly associated with the MAPK/ERK, JAK/STAT3, and PI3K/AKT signaling pathways in COAD cells.…”

Section: Discussionmentioning

confidence: 99%

KLF7 promotes colon adenocarcinoma progression through the PDGFB signaling pathway

Zhang,

Jiang,

et al. 2024

Int. J. Biol. Sci.

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Colon adenocarcinoma (COAD) is the most common malignancy of the digestive tract, which is characterized by a dismal prognosis. No effective treatment has been established presently, thus there is an urgent need to understand the mechanisms driving COAD progression in order to develop effective therapeutic approaches and enhance clinical outcomes. In this study, we found that KLF7 is overexpressed in COAD tissues and correlated with clinicopathological features of COAD. Both gain-of-function and loss-of-function experiments have unequivocally demonstrated that overexpression of KLF7 promotes the growth and metastasis of COAD in vitro and in vivo , while KLF7 knockdown attenuated these effects. Mechanistically, our findings reveal that KLF7 can specifically bind to the promoter region of PDGFB (TGGGTGGAG), thus promoting the transcription of PDGFB and increasing its secretion. Subsequently, secreted PDGFB facilitates the progression of COAD by activating MAPK/ERK, PI3K/AKT, and JAK/STAT3 signaling pathways through PDGFRβ. Additionally, we found that sunitinib can block PDGFB signaling and inhibit COAD progression, offering a promising therapeutic strategy for COAD treatment.

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Section: Discussionmentioning

confidence: 99%

KLF7 promotes colon adenocarcinoma progression through the PDGFB signaling pathway

Zhang,

Jiang,

et al. 2024

Int. J. Biol. Sci.

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“…Furthermore, PDGF-D promotes EMT transformation in colorectal cancer via activation of Notch1/Twist1 pathway [ 68 ]. In addition to PDGF-D, PDGF-B not only contributes to EMT in gastric cancer cells by activating MAPK/ERK pathway [ 69 ], but also promotes the expression of zinc finger E-box binding homeobox 1 (ZEB1) by downregulating the expression of miR-200 in triple negative breast cancer [ 70 ].…”

Section: Activated Platelets Promote Tumor Cell Emtmentioning

confidence: 99%

Platelets involved tumor cell EMT during circulation: communications and interventions

et al. 2022

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Distant spreading of metastatic tumor cells is still the leading cause of tumor death. Metastatic spreading is a complex process, in which epithelial-mesenchymal transition (EMT) is the primary and key event to promote it. Presently, extensive reviews have given insights on the occurrence of EMT at the primary tumor site that depends on invasive properties of tumor cells and the tumor-associated microenvironment. However, essential roles of circulation environment involved in tumor cell EMT is not well summarized. As a main constituent of the blood, platelet is increasingly found to work as an important activator to induce EMT. Therefore, this review aims to emphasize the novel role of platelet in EMT through signal communications between platelets and circulation tumor cells, and illustrate potent interventions aiming at their communications. It may give a complementary view of EMT in addition to the tissue microenvironment, help for better understand the hematogenous metastasis, and also illustrate theoretical and practical basis for the targeted inhibition.

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Putative epithelial–mesenchymal transitions during salamander limb regeneration: Current perspectives and future investigations

Kim,

Whited

2024

Annals of the New York Academy of Sciences

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Previous studies have implicated epithelial–mesenchymal transition (EMT) in salamander limb regeneration. In this review, we describe putative roles for EMT during each stage of limb regeneration in axolotls and other salamanders. We hypothesize that EMT and EMT‐like gene expression programs may regulate three main cellular processes during limb regeneration: (1) keratinocyte migration during wound closure; (2) transient invasion of the stump by epithelial cells undergoing EMT; and (3) use of EMT‐like programs by non‐epithelial blastemal progenitor cells to escape the confines of their niches. Finally, we propose nontraditional roles for EMT during limb regeneration that warrant further investigation, including alternative EMT regulators, stem cell activation, and fibrosis induced by aberrant EMT.

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Platelet-derived growth factor-B signalling might promote epithelial-mesenchymal transition in gastric carcinoma cells through activation of the MAPK/ERK pathway

Cited by 3 publications

References 40 publications

KLF7 promotes colon adenocarcinoma progression through the PDGFB signaling pathway

KLF7 promotes colon adenocarcinoma progression through the PDGFB signaling pathway

Platelets involved tumor cell EMT during circulation: communications and interventions

Putative epithelial–mesenchymal transitions during salamander limb regeneration: Current perspectives and future investigations

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