ELTD1 Promotes Gastric Cancer Cell Proliferation, Invasion and Epithelial–Mesenchymal Transition Through MAPK/ERK Signaling by Regulating CSK

Sun, Bo; Zhong, Fang-Jing

doi:10.2147/ijgm.s325495

Cited by 4 publications

(6 citation statements)

References 32 publications

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“…These results demonstrate that sumoylation of CSK negatively modulates its tumor suppressor function by reducing its interaction with CBP and therefore causing Src activation (Cui et al, 2019). ELTD1 also can interact with and lower the level of CSK which leads to Src activation and MAPK activation (Sun and Zhong, 2021).…”

Section: Regulation Of Cskmentioning

confidence: 75%

“…It has been found that ELTD1 is not only significantly elevated in gastric cancer cells, but also plays a pivotal role in tumor growth and metastasis of gastric cancer due to its involvement in proliferation, migration, invasion, and epithelial-mesenchymal transition. Mechanistically, by interacting with and downregulating CSK, elevated ELTD1 leads to activation of both Src and MAPK (Sun and Zhong, 2021). Bioinformatic analysis found that high ELTD1 levels combing low CSK levels gives the best predicting performance (Sun and Zhong, 2021).…”

Section: Csk In Cancermentioning

confidence: 99%

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Regulation, targets and functions of CSK

Zhu

Wang

Ranjan

et al. 2023

Front. Cell Dev. Biol.

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The Src family kinases (SFK) plays an important role in multiple signal transduction pathways. Aberrant activation of SFKs leads to diseases such as cancer, blood disorders, and bone pathologies. By phosphorylating and inactivating SFKs, the C-terminal Src kinase (CSK) serves as the key negative regulator of SFKs. Similar to Src, CSK is composed of SH3, SH2, and a catalytic kinase domain. However, while the Src kinase domain is intrinsically active, the CSK kinase domain is intrinsically inactive. Multiple lines of evidence indicate that CSK is involved in various physiological processes including DNA repair, permeability of intestinal epithelial cells (IECs), synaptic activity, astrocyte-to-neuron communication, erythropoiesis, platelet homeostasis, mast cell activation, immune and inflammation responses. As a result, dysregulation of CSK may lead to many diseases with different underlying molecular mechanisms. Furthermore, recent findings suggest that in addition to the well-established CSK-SFK axis, novel CSK-related targets and modes of CSK regulation also exist. This review focuses on the recent progress in this field for an up-to-date understanding of CSK.

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Section: Regulation Of Cskmentioning

confidence: 75%

Section: Csk In Cancermentioning

confidence: 99%

Regulation, targets and functions of CSK

Zhu

Wang

Ranjan

et al. 2023

Front. Cell Dev. Biol.

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“…The MAPK signaling pathway represents another signaling pathway involved in EMT, which includes ERK1/2, and Bao et al (2021) recently reported that a member of the erythrocyte membrane protein band 4.1 superfamily, EPB41L5, overexpressed in esophageal cancer, activated the phosphorylation of ERK/p38 signaling pathway components. Two additional reports have shown the involvement of two other proteins in the activation of this pathway, the seven-transmembrane domain-containing 1 (ELTD1) (Sun and Zhong, 2021), and actin gamma 1 (ACTG1) (Xiao et al, 2021). Concerning PI3K/Akt/mTOR signaling, which regulates the EMT of gastric cancer cells, its aberrant phosphorylation was found to be caused by cooperation between CD36 and apolipoprotein C2 (APOC2) .…”

Section: Major Findings Relevant To Other Signaling Pathwaysmentioning

confidence: 99%

Curcuminoids as Modulators of EMT in Invasive Cancers: A Review of Molecular Targets With the Contribution of Malignant Mesothelioma Studies

et al. 2022

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Curcuminoids, which include natural acyclic diarylheptanoids and the synthetic analogs of curcumin, have considerable potential for fighting against all the characteristics of invasive cancers. The epithelial-to-mesenchymal transition (EMT) is a fundamental process for embryonic morphogenesis, however, the last decade has confirmed it orchestrates many features of cancer invasiveness, such as tumor cell stemness, metabolic rewiring, and drug resistance. A wealth of studies has revealed EMT in cancer is in fact driven by an increasing number of parameters, and thus understanding its complexity has now become a cornerstone for defining future therapeutic strategies dealing with cancer progression and metastasis. A specificity of curcuminoids is their ability to target multiple molecular targets, modulate several signaling pathways, modify tumor microenvironments and enhance the host’s immune response. Although the effects of curcumin on these various parameters have been the subject of many reviews, the role of curcuminoids against EMT in the context of cancer have never been reviewed so far. This review first provides an updated overview of all EMT drivers, including signaling pathways, transcription factors, non-coding RNAs (ncRNAs) and tumor microenvironment components, with a special focus on the most recent findings. Secondly, for each of these drivers the effects of curcumin/curcuminoids on specific molecular targets are analyzed. Finally, we address some common findings observed between data reported in the literature and the results of investigations we conducted on experimental malignant mesothelioma, a model of invasive cancer representing a useful tool for studies on EMT and cancer.

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“…In this regard, Sun et al found epidermal growth factor, latrophilin and seven transmembrane domain-containing protein 1’s (ELTD1) expression is heightened in gastric cancer. ELTD1 is a G-protein-coupled receptor usually playing a role in angiogenesis, cellular metabolism and cardiac hypertrophy ( Sun and Zhong, 2021 ). In tumors, interaction of ELTD1 with CSK inhibits CSK function, thus promoting MAPK/ERK signaling which leads to increased cell proliferation, epithelial to mesenchymal transition and metastasis ( Sun and Zhong, 2021 ).…”

Section: Clinical Importance Of Tyrosine-protein Kinase Cskmentioning

confidence: 99%

“…ELTD1 is a G-protein-coupled receptor usually playing a role in angiogenesis, cellular metabolism and cardiac hypertrophy ( Sun and Zhong, 2021 ). In tumors, interaction of ELTD1 with CSK inhibits CSK function, thus promoting MAPK/ERK signaling which leads to increased cell proliferation, epithelial to mesenchymal transition and metastasis ( Sun and Zhong, 2021 ).…”

Section: Clinical Importance Of Tyrosine-protein Kinase Cskmentioning

confidence: 99%

Apoptosis regulation by the tyrosine-protein kinase CSK

Fortner

Chera

Tanca

et al. 2022

Front. Cell Dev. Biol.

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C-terminal Src kinase (CSK) is a cytosolic tyrosine-protein kinase with an important role in regulating critical cellular decisions, such as cellular apoptosis, survival, proliferation, cytoskeletal organization and many others. Current knowledge on the CSK mechanisms of action, regulation and functions is still at an early stage, most of CSK’s known actions and functions being mediated by the negative regulation of the SRC family of tyrosine kinases (SFKs) through phosphorylation. As SFKs play a vital role in apoptosis, cell proliferation and survival regulation, SFK inhibition by CSK has a pro-apoptotic effect, which is mediated by the inhibition of cellular signaling cascades controlled by SFKs, such as the MAPK/ERK, STAT3 and PI3K/AKT signaling pathways. Abnormal functioning of CSK and SFK activation can lead to diseases such as cancer, cardiovascular and neurological manifestations. This review describes apoptosis regulation by CSK, CSK inhibition of the SFKs and further explores the clinical relevance of CSK in important pathologies, such as cancer, autoimmune, autoinflammatory, neurologic diseases, hypertension and HIV/AIDS.

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ELTD1 Promotes Gastric Cancer Cell Proliferation, Invasion and Epithelial–Mesenchymal Transition Through MAPK/ERK Signaling by Regulating CSK

Cited by 4 publications

References 32 publications

Regulation, targets and functions of CSK

Regulation, targets and functions of CSK

Curcuminoids as Modulators of EMT in Invasive Cancers: A Review of Molecular Targets With the Contribution of Malignant Mesothelioma Studies

Apoptosis regulation by the tyrosine-protein kinase CSK

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