NEDD9 promotes invasion and migration of colorectal cancer cell line HCT116 via JNK/EMT

Meng, Haining; Wu, Junyu; Huang, Qiao; Yang, Xi; Yang, Kunao; Qiu, Yuexin; Ji-wen, Ren; Shen, Ruowu; Hong, Quan

doi:10.3892/ol.2019.10756

Cited by 12 publications

(16 citation statements)

References 43 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Consistent with this, knockdown of NKCC1 inhibited EMT-related proteins including Snail, vimentin, MMP2 and MMP9 but increased E-cadherin, while NKCC1 overexpression had the opposite effects. Several studies have shown that JNK promoted EMT and enhanced the invasion and migration of GC cells 24 , 38 - 40 , which was consistent with our findings. Furthermore, NKCC1 silencing also inhibited JNK activation without affecting P-38 and ERK.…”

Section: Discussionsupporting

confidence: 93%

“…EMT not only initiates tumor invasion and migration, but is also an indicator of the distant metastasis ability of tumor cells 36 - 37 . Studies show that EMT promotes GC progression via the MAPK-JNK signaling pathway, and activating this pathway induces tumor EMT 38 - 40 . Consistent with this, knockdown of NKCC1 inhibited EMT-related proteins including Snail, vimentin, MMP2 and MMP9 but increased E-cadherin, while NKCC1 overexpression had the opposite effects.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

NKCC1 promotes proliferation, invasion and migration in human gastric cancer cells via activation of the MAPK-JNK/EMT signaling pathway

Wang¹,

Zhao²,

Chen³

et al. 2021

J. Cancer

View full text Add to dashboard Cite

Aims: This study aimed to explore the function of NKCC1 in the proliferation, migration and invasion of Gastric cancer (GC) cells. Materials and Methods: GC data extracted from the database was analyzed using molecular bioinformatics. The expression levels of NKCC1 in tissue samples from GC patients and GC cell lines were determined by Western blotting, qRT-PCR, and immunohistochemistry. Immunofluorescence was used to detect protein localization. The GC cell lines were transfected with NKCC1-shRNA or expression plasmid, and in vitro proliferation, invasion and migration were analyzed by the CCK8, wound healing and transwell tests. Results: The NKCC1 mRNA level was significantly increased in GC tissues than that in normal gastric tissues ( P = 0.0195). This phenomenon was further confirmed by the analysis of the TCGA-GTEx database that includes 408 gastric cancer tissues and 211 normal gastric tissues ( P < 0.01). Furthermore, the increased level of NKCC1 was significantly correlated with Tumor size ( P = 0.039), lymphatic node metastasis ( P = 0.035) and tumor stage ( P = 0.034). In vitro experiments confirmed that NKCC1 expression was higher in GC cells compared to that in GES-1 cells, and was mainly localized to the cytoplasm and membrane. NKCC1 silencing inhibited GC cell proliferation, invasion, migration and EMT, whereas its overexpression had the opposite effects. Furthermore, NKCC1 overexpression upregulated and activated JNK, and the targeted inhibition of JNK by SP600125 abrogated the pro-metastatic effects of NKCC1. Conclusions: NKCC1 promotes migration and invasion of GC cells by MAPK-JNK/EMT pathway and can be a potential therapeutic target.

show abstract

Section: Discussionsupporting

confidence: 93%

Section: Discussionmentioning

confidence: 99%

NKCC1 promotes proliferation, invasion and migration in human gastric cancer cells via activation of the MAPK-JNK/EMT signaling pathway

Wang¹,

Zhao²,

Chen³

et al. 2021

J. Cancer

View full text Add to dashboard Cite

show abstract

“…The inhibition of JNK led to the upregulation of E-cadherin and the downregulation of Vimentin and Slug in AR-independent PCa cells PC-3 and DU145. These results were similar to previous studies, which showed that inhibition of JNK decreased EMT in HCT116 colon carcinoma cells [55]. JNK inhibition was shown to decrease hypoxia-mediated EMT transition and stemness properties in HT29 and SW-480 colon carcinoma cells [56].…”

Section: Jnk and Wnt-11 Presented Similar Functional Properties In Thsupporting

confidence: 92%

Inhibition on JNK Mimics Silencing of Wnt-11 Mediated Cellular Response in Androgen-Independent Prostate Cancer Cells

Arısan

Rencüzoğulları

Keskin

et al. 2020

Biology

View full text Add to dashboard Cite

Prostate cancer (PCa) is one of the most common cancers among men, and one of the leading causes of cancer death for men. The c-Jun N-terminal kinase (JNK) pathway is required for several cellular functions, such as survival, proliferation, differentiation, and migration. Wnt-11, a member of the Wnt family, has been identified for its upregulation in PCa; however, downstream signalling of Wnt-11 remains to be fully characterized. In this study, we investigated the role of the JNK pathway as a potential downstream factor for Wnt-11 signalling. For this purpose, LNCaP, DU145, and PC-3 PCa cells and normal epithelial PNT1A cells were treated with a specific JNK kinase inhibitor: JNKVIII. Our results showed that JNK inhibition decreased mitochondrial membrane potential and promoted cell death in a cell type-dependent manner. We found that JNK inhibition led to an increase in autophagy and prevented epithelial–mesenchymal transition (EMT) in independently growing androgen cells. JNK inhibition and the silencing of Wnt-11 showed similar responses in DU145 and PC-3 cells and decreased metastasis-related biomarkers, cell migration, and invasion. Overall, our results suggest that JNK signalling plays a significant role in the pathophysiology of PCa by mediating Wnt-11 induced signals. Our data highlights that both the JNK pathway and Wnt-11 could be a useful therapeutic target for the combinatory application of current PCa.

show abstract

“…Furthermore, JNK may be associated with Snail and TWIST1 via c-Jun in multi-drug resistant epidermoid carcinoma and as a downstream effector of Akt in gastric cancer cells (120,121). Other researches also associated JNK with EMT induction in colorectal cancer (122) and non-small cell lung cancer cells (123). Whereas, for p38 MAPK-mediated EMT, Lin et al (124) evaluated that p38 MAPK regulated p38 interacting protein (p38IP) and Snail in head and neck squamous cell carcinoma.…”

Section: Mapksmentioning

confidence: 97%

Hypoxia-Induced Epithelial-Mesenchymal Transition in Cancers: HIF-1α and Beyond

2020

View full text Add to dashboard Cite

Metastasis is the main cause of cancer-related mortality. Although the actual process of metastasis remains largely elusive, epithelial-mesenchymal transition (EMT) has been considered as a major event in metastasis. Besides, hypoxia is common in solid cancers and has been considered as an important factor for adverse treatment outcomes including metastasis. Since EMT and hypoxia potentially share several signaling pathways, many recent studies focused on investigate the issue of hypoxia-induced EMT. Among all potential mediators of hypoxia-induced EMT, hypoxia-inducible factor-1α (HIF-1α) has been studied extensively. Moreover, there are other potential mediators that may also contribute to the process. This review aims to summarize the recent reports on hypoxia-induced EMT by HIF-1α or other potential mediators and provide insights for further investigations on this issue. Ultimately, better understanding of hypoxia-induced EMT may allow us to develop anti-metastatic strategies and improve treatment outcomes.

show abstract

NEDD9 promotes invasion and migration of colorectal cancer cell line HCT116 via JNK/EMT

Cited by 12 publications

References 43 publications

NKCC1 promotes proliferation, invasion and migration in human gastric cancer cells via activation of the MAPK-JNK/EMT signaling pathway

NKCC1 promotes proliferation, invasion and migration in human gastric cancer cells via activation of the MAPK-JNK/EMT signaling pathway

Inhibition on JNK Mimics Silencing of Wnt-11 Mediated Cellular Response in Androgen-Independent Prostate Cancer Cells

Hypoxia-Induced Epithelial-Mesenchymal Transition in Cancers: HIF-1α and Beyond

Contact Info

Product

Resources

About