Tripartite motif containing 25 promotes proliferation and invasion of colorectal cancer cells through TGF-β signaling

Tripartite motif containing 25 (TRIM25) is a member of TRIM proteins and functions as an E3 (ubiquitin ligase). It has been found to act as an oncogene in gastric cancer cells and is abnormally expressed in cancers in female reproductive system. Here, we investigated the function of TRIM25 in colorectal cancer. TRIM25 was found to be significantly up-regulated in colorectal cancer tissues and cancer cell lines through real-time PCR assay. Colorectal cancer cells (CRCs) overexpressing TRIM25 exhibited a two-fold higher proliferation and migration rate compared with their parental lines in vitro. Moreover, TRIM25 also promoted tumor progression in vivo. Further study indicated that TRIM25 worked through positively regulating transforming growth factor β (TGF-β) signaling pathway to regulate the proliferation and invasion of CRCs. In summary, our results indicate that TRIM25 also acts as an oncogene in colorectal cancer and it functions through TGF-β signaling pathway. Thus, TRIM25 represents potential targets for the treatment of colorectal cancer.

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Salinomycin and Sulforaphane Exerted Synergistic Antiproliferative and Proapoptotic Effects on Colorectal Cancer Cells by Inhibiting the PI3K/Akt Signaling Pathway in vitro and in vivo

OncoTargets and Therapy ◽

10.2147/ott.s246706 ◽

2020 ◽

Vol Volume 13 ◽

pp. 4957-4969

Author(s):

Fang Liu ◽

Rong-Bin Lv ◽

Yan Liu ◽

Qian Hao ◽

Shu-Jie Liu ◽

...

Keyword(s):

Colorectal Cancer ◽

Cancer Cells ◽

Signaling Pathway ◽

Akt Signaling ◽

Akt Signaling Pathway ◽

Colorectal Cancer Cells

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Pristimerin exhibits in vitro and in vivo anticancer activities through inhibition of nuclear factor-кB signaling pathway in colorectal cancer cells

Phytomedicine ◽

10.1016/j.phymed.2018.01.008 ◽

2018 ◽

Vol 40 ◽

pp. 140-147 ◽

Cited By ~ 13

Author(s):

Bashir A. Yousef ◽

Hozeifa M. Hassan ◽

Lu-Yong Zhang ◽

Zhen-Zhou Jiang

Keyword(s):

Colorectal Cancer ◽

Cancer Cells ◽

Signaling Pathway ◽

Nuclear Factor ◽

Anticancer Activities ◽

Colorectal Cancer Cells

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Dehydrodiisoeugenol inhibits colorectal cancer growth by endoplasmic reticulum stress-induced autophagic pathways

Journal of Experimental & Clinical Cancer Research ◽

10.1186/s13046-021-01915-9 ◽

2021 ◽

Vol 40 (1) ◽

Author(s):

Changhong Li ◽

Kui Zhang ◽

Guangzhao Pan ◽

Haoyan Ji ◽

Chongyang Li ◽

...

Keyword(s):

Colorectal Cancer ◽

Endoplasmic Reticulum ◽

Cell Growth ◽

Er Stress ◽

Cancer Cells ◽

Tumor Xenograft ◽

Anticancer Activities ◽

Colorectal Cancer Cells

Abstract Background Dehydrodiisoeugenol (DEH), a novel lignan component extracted from nutmeg, which is the seed of Myristica fragrans Houtt, displays noticeable anti-inflammatory and anti-allergic effects in digestive system diseases. However, the mechanism of its anticancer activity in gastrointestinal cancer remains to be investigated. Methods In this study, the anticancer effect of DEH on human colorectal cancer and its underlying mechanism were evaluated. Assays including MTT, EdU, Plate clone formation, Soft agar, Flow cytometry, Electron microscopy, Immunofluorescence and Western blotting were used in vitro. The CDX and PDX tumor xenograft models were used in vivo. Results Our findings indicated that treatment with DEH arrested the cell cycle of colorectal cancer cells at the G1/S phase, leading to significant inhibition in cell growth. Moreover, DEH induced strong cellular autophagy, which could be inhibited through autophagic inhibitors, with a rction in the DEH-induced inhibition of cell growth in colorectal cancer cells. Further analysis indicated that DEH also induced endoplasmic reticulum (ER) stress and subsequently stimulated autophagy through the activation of PERK/eIF2α and IRE1α/XBP-1 s/CHOP pathways. Knockdown of PERK or IRE1α significantly decreased DEH-induced autophagy and retrieved cell viability in cells treated with DEH. Furthermore, DEH also exhibited significant anticancer activities in the CDX- and PDX-models. Conclusions Collectively, our studies strongly suggest that DEH might be a potential anticancer agent against colorectal cancer by activating ER stress-induced inhibition of autophagy.

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A novel inhibitor of ADAM17 sensitizes colorectal cancer cells to 5-Fluorouracil by reversing Notch and epithelial-mesenchymal transition in vitro and in vivo

Cell Proliferation ◽

10.1111/cpr.12480 ◽

2018 ◽

Vol 51 (5) ◽

pp. e12480 ◽

Cited By ~ 13

Author(s):

Dan-Dan Li ◽

Chang-Hao Zhao ◽

Huai-Wei Ding ◽

Qiong Wu ◽

Tian-Shu Ren ◽

...

Keyword(s):

Colorectal Cancer ◽

Cancer Cells ◽

Epithelial Mesenchymal Transition ◽

Mesenchymal Transition ◽

Colorectal Cancer Cells

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Apelin Over-Expression Promotes Proliferation and Angiogenesis of Gastric Cancer Cells

10.21203/rs.3.rs-530677/v2 ◽

2021 ◽

Author(s):

Li-Jun Tian ◽

Hong-Zhi Liu ◽

Qiang Zhang ◽

Dian-Zhong Geng ◽

Jing Yang ◽

...

Keyword(s):

Gastric Cancer ◽

Cyclin D1 ◽

Cancer Cells ◽

Signaling Pathway ◽

Cox Regression ◽

Gastric Cancer Cells ◽

Over Expression ◽

Normal Tissues

Abstract Background: Apelin is a recently identified endogenous ligand associated with proliferation and angiogenesis of several cancers. However, only few studies have reported on the functions and the role of apelin in gastric cancer (GC). Therefore, in the present study, we investigated the association and the mechanisms underlying Apelin expression and proliferation of GC cells both in vitro and in vivo.Methods: We enrolled 178 postoperative care GC patients to investigate clinicopathological and immunohistochemical factors associated with Apelin expression. The relationship between Survival of patients and apelin expression was evaluated using Kaplan-Meier method and Cox regression analyses. The expression of apelin mRNA and its proteins in GC tissues and cell lines were analyzed using quantitative real-time reverse transcription-polymerase chain reaction (RT-PCR), western blot and ELISA. The role and mechanisms underlying regulation of Apelin expression in human GC cells were evaluated through several in vitro and in vivo experiments. Results: Apelin was over expressed in human GC cells, relative to adjacent normal tissues. The over expression of apelin was associated with vessel invasion (P <0.01), lymph node metastasis (P <0.01), late-staged tumor (T) (P <0.05), worse pathological type (P <0.05), nerve invasion (P <0.05). In addition, expression of apelin strongly and positively correlated with that of vascular endothelial growth factor (VEGF). Over-expression of apelin promoted proliferation and invasion of MGC-803 cell via the ERK/Cyclin D1/MMP-9 signaling pathway. Apelin over-expression also promoted angiogenesis of GC cells, accelerating growth of subcutaneous xenograft of the cancer cells in vivo.Conclusions: Over-expression of apelin promotes proliferation and metastasis of GC cells via the ERK/Cyclin D1/MMP-9 signaling pathway and is associated with adverse events of the cancer. Consequently, apelin is a potential therapeutic target for human GC.

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