TKP, a serine protease extracted from Trichosanthes kirilowii , inhibits the migration and invasion of colorectal adenocarcinoma cells by targeting Wnt/β‐catenin and Hedgehog/Gli1 signalings

2019 ◽  
Vol 34 (4) ◽  
pp. 867-878
Author(s):  
Xiaomei Sun ◽  
Xiaobo Xu ◽  
Li Song
2016 ◽  
Vol 7 (2) ◽  
pp. 843-854 ◽  
Author(s):  
Li Song ◽  
Jiao Chang ◽  
Zhuoyu Li

A novel protein TKP extracted from T. kirilowii fruit exerted potential anti-colorectal cancer activity by inducing apoptosis, which was regulated by the PI3K/AKT-mediated mitochondria-dependent pathway.


2019 ◽  
Vol Volume 12 ◽  
pp. 6789-6795 ◽  
Author(s):  
Fei Liu ◽  
Jianhui Jia ◽  
Liping Sun ◽  
Qingrui Yu ◽  
Hongyan Duan ◽  
...  

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Jiguang Meng ◽  
Xuxin Chen ◽  
Zhihai Han

Abstract Background To investigate the role and its potential mechanism of 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase 4 (PFKFB4) in lung adenocarcinoma. Methods Co-immunoprecipitation was performed to analyze the interaction between PFKFB4 and SRC-2. Western blot was used to investigate the phosphorylation of steroid receptor coactivator-2 (SRC-2) on the condition that PFKFB4 was knockdown. Transcriptome sequencing was performed to find the downstream target of SRC-2. Cell Counting Kit-8 (CCK-8) assay, transwell assay and transwell-matrigel assay were used to examine the proliferation, migration and invasion abilities in A549 and NCI-H1975 cells with different treatment. Results In our study we found that PFKFB4 was overexpressed in lung adenocarcinoma associated with SRC family protein and had an interaction with SRC-2. PFKFB4 could phosphorylate SRC-2 at Ser487, which altered SRC-2 transcriptional activity. Functionally, PFKFB4 promoted lung adenocarcinoma cells proliferation, migration and invasion by phosphorylating SRC-2. Furthermore, we identified that CARM1 was transcriptionally regulated by SRC-2 and involved in PFKFB4-SRC-2 axis on lung adenocarcinoma progression. Conclusions Our research reveal that PFKFB4 promotes lung adenocarcinoma cells proliferation, migration and invasion via enhancing phosphorylated SRC-2-mediated CARM1 expression.


2010 ◽  
Vol 397 (2) ◽  
pp. 214-219 ◽  
Author(s):  
Akira Shibata ◽  
Kiyotaka Nakagawa ◽  
Phumon Sookwong ◽  
Tsuyoshi Tsuduki ◽  
Akira Asai ◽  
...  

Molecules ◽  
2012 ◽  
Vol 17 (6) ◽  
pp. 6633-6657 ◽  
Author(s):  
Chim Kei Chan ◽  
Bey Hing Goh ◽  
Muhamad Noor Alfarizal Kamarudin ◽  
Habsah Abdul Kadir

Molecules ◽  
2021 ◽  
Vol 26 (23) ◽  
pp. 7375
Author(s):  
Paulina Lewandowska ◽  
Izabela Szczuka ◽  
Iwona Bednarz-Misa ◽  
Berenika M. Szczęśniak-Sięga ◽  
Katarzyna Neubauer ◽  
...  

The mechanisms underlying the antineoplastic effects of oxicams have not been fully elucidated. We aimed to assess the effect of classic and novel oxicams on the expression/secretion of macrophage-associated chemokines (RTqPCR/Luminex xMAP) in colorectal adenocarcinoma cells, and on the expression of upstream the non-steroidal anti-inflammatory drug (NSAID)-activated genes NAG1, NFKBIA, MYD88, and RELA, as well as at the chemokine profiling in colorectal tumors. Meloxicam downregulated CCL4 9.9-fold, but otherwise the classic oxicams had a negligible/non-significant effect. Novel analogues with a thiazine ring substituted with arylpiperazine and benzoyl moieties significantly modulated chemokine expression to varying degree, upregulated NAG1 and NFKBIA, and downregulated MYD88. They inhibited CCL3 and CCL4, and their effect on CCL2 and CXCL2 depended on the dose and exposure. The propylene linker between thiazine and piperazine nitrogens and one arylpiperazine fluorine substituent characterized the most effective analogue. Only CCL19 and CXCL2 were not upregulated in tumors, nor was CXCL2 in tumor-adjacent tissue compared to normal mucosa. Compared to adjacent tissue, CCL4 and CXCL2 were upregulated, while CCL2, CCL8, and CCL19 were downregulated in tumors. Tumor CCL2 and CCL7 increased along with advancing T and CCL3, and CCL4 along with the N stage. The introduction of arylpiperazine and benzoyl moieties into the oxicam scaffold yields effective modulators of chemokine expression, which act by upregulating NAG1 and interfering with NF-κB signaling.


2021 ◽  
Vol 2021 ◽  
pp. 1-10
Author(s):  
Qin Yu ◽  
Jianzhang Wang ◽  
Tiantian Li ◽  
Xinxin Xu ◽  
Xinyue Guo ◽  
...  

Endometrial adenocarcinoma is one of the most prevalent female reproductive tract cancers in the world, and the development of effective treatment is still the main goal of its current research. Epithelial-mesenchymal transition (EMT) plays a significant part in the occurrence and development of epithelial carcinoma, including endometrial adenocarcinoma. Recepteur d’origine nantais (RON) induces EMT and promotes proliferation, migration, and invasion in various epithelial-derived cancers, but its role in endometrial adenocarcinoma is still poorly studied. The purpose of this study is to verify the overexpression of RON in endometrial adenocarcinoma and to explore its specific roles. RON expression in tumor lesions was verified by immunohistochemical staining, HEC-1B cells were used to construct stable cell lines with RON overexpression or knockdown to investigate the effects of RON on the function of endometrial adenocarcinoma cells, and xenotransplantation experiment was carried out in nude mice to explore the effect of RON on the growth of endometrial adenocarcinoma in vivo. This study revealed that RON could promote the proliferation, migration, and invasion of HEC-1B cells and induce EMT, and these effects were regulated through the Smad pathway. RON overexpression could promote growth of endometrial adenocarcinoma cells in nude mice, while its inhibitor BMS777607 could restrict this role. RON played an important role in endometrial adenocarcinoma and had a potential to become a new therapeutic target for endometrial adenocarcinoma.


2019 ◽  
Vol 24 (2) ◽  
pp. 187-196
Author(s):  
José Javier Zamorano-León ◽  
Sandra Ballesteros ◽  
Natalia de las Heras ◽  
Luis Alvarez-Sala ◽  
Mariano de la Serna-Soto ◽  
...  

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