Upregulation of microRNA-135b and microRNA-182 promotes chemoresistance of colorectal cancer by targeting ST6GALNAC2 via PI3K/AKT pathway

2017 ◽  
Vol 56 (12) ◽  
pp. 2669-2680 ◽  
Author(s):  
Bing Liu ◽  
Yanfeng Liu ◽  
Lifen Zhao ◽  
Yue Pan ◽  
Yujia Shan ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Akt Pathway

PGM1 Suppresses Colorectal Cancer Cell Migration And Invasion by Regulating PI3K/ AKT Pathway

2021 ◽  
Author(s):  
Zhewen Zheng ◽  
Xue Zhang ◽  
Jian Bai ◽  
Long Long ◽  
Di Liu ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cell Cycle ◽  
Colony Formation ◽  
Tumor Formation ◽  
Akt Pathway ◽  
Migration And Invasion ◽  
Cycle Arrest ◽  
Cancer Pathogenesis

Abstract BackgroundPhosphoglucomutase 1(PGM1) is known for its involvement in cancer pathogenesis. However, its biological role in colorectal cancer (CRC) is unknown. Here, we studied the functions and mechanisms of PGM1 in CRC.Methods We verified PGM-1 as a DEG by a comprehensive strategy of the TCGA-COAD dataset mining and computational biology. Relative levels of PGM-1 in CRC tumors and adjoining peritumoral tissue were identified by qRT-PCR, WB, and IHC staining in a tissue microarray. PGM1 functions were analyzed using CCK8, EdU, colony formation, cell cycle, apoptosis, and Transwell migration and invasion assays. The influence of PGM1 was further investigated using tumor formation in vivo.ResultsPGM1 mRNA and protein were both reduced in CRC and the reduction was related to CRC pathology and overall survival. PGM1 knockdown stimulated both proliferation and colony formation, promoting cell cycle arrest and apoptosis while overexpression has opposite effects in CRC cells both in vivo and in vitro. Furthermore, we lined the actions of PGM1 to the PI3K/ AKT pathway. ConclusionWe verified that PGM1 suppresses CRC through the PI3K/ AKT pathway. These results suggest the potential for targeting PGM1 in CRC therapies.

scholarly journals Author Correction: Verbascoside: Identification, Quantification, and Potential Sensitization of Colorectal Cancer Cells to 5-FU by Targeting PI3K/AKT Pathway

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Yasmeen M. Attia ◽  
Dina M. El-Kersh ◽  
Hebatallah A. Wagdy ◽  
Mohamed M. Elmazar
Keyword(s):  
Colorectal Cancer ◽  
Cancer Cells ◽  
Akt Pathway ◽  
Colorectal Cancer Cells

An amendment to this paper has been published and can be accessed via a link at the top of the paper.

Metformin inhibits β-catenin phosphorylation on Ser-552 through an AMPK/PI3K/Akt pathway in colorectal cancer cells

2019 ◽  
Vol 112 ◽  
pp. 88-94 ◽  
Author(s):  
Gastón Amable ◽  
Eduardo Martínez-León ◽  
María Elisa Picco ◽  
Nicolas Di Siervi ◽  
Carlos Davio ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cancer Cells ◽  
Akt Pathway ◽  
Colorectal Cancer Cells

NEDD4 is overexpressed in colorectal cancer and promotes colonic cell growth independently of the PI3K/PTEN/AKT pathway

2013 ◽  
Vol 25 (1) ◽  
pp. 12-18 ◽  
Author(s):  
Peter W. Eide ◽  
Lina Cekaite ◽  
Stine A. Danielsen ◽  
Ina A. Eilertsen ◽  
Ane Kjenseth ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cell Growth ◽  
Akt Pathway

scholarly journals Loss of Smad4 in colorectal cancer induces resistance to 5-fluorouracil through activating Akt pathway

2014 ◽  
Vol 110 (4) ◽  
pp. 946-957 ◽  
Author(s):  
B Zhang ◽  
B Zhang ◽  
X Chen ◽  
S Bae ◽  
K Singh ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Akt Pathway

Molecular characteristics of complete PTEN loss in metastatic colorectal cancer.

2013 ◽  
Vol 31 (4_suppl) ◽  
pp. 389-389
Author(s):  
Zhi-Qin Jiang ◽  
Laurel Deaton ◽  
Nastaran Neishaboori ◽  
Jean-Nicolas Vauthey ◽  
Michael J. Overman ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Metastatic Colorectal Cancer ◽  
Cpg Island ◽  
Pik3ca Mutation ◽  
The Cancer Genome Atlas ◽  
Akt Pathway ◽  
Molecular Characteristics ◽  
Braf Mutations ◽  
Pik3ca Mutations ◽  
Pten Loss

389 Background: Loss of expression of phosphatase and tensin homolog (PTEN) is associated with activation of the PI3K/AKT pathway, and has been identified as a potential modulator of response to targeted therapies in metastatic colorectal cancer (mCRC). The association of PTEN loss with other molecular characteristics and outcomes has not been described for mCRC. Methods: Tumor from 229 mCRC patients (pts) were included for analysis of PTEN staining by IHC from whole-mounts, across two cohorts of unresectable mCRC or resectable liver-limited disease. PTEN loss was defined as complete loss of staining with preservation of expression of stromal components. Mutation status was defined using mass-spectroscopy or next-generation sequencing platforms. CpG island methylation (CIMP) status was determined using a previously defined 6-marker panel, with methylation of ≥3 markers denoting CIMP-High. Methylation findings where confirmed in 193 pts from the Cancer Genome Atlas (TCGA) database, using previously defined classifications. Results: The overall frequency of complete PTEN loss was 12% in the primary tumor and 15% when assayed from metastatic sites (P=NS). There was no difference in clinical characteristics in patients with PTEN-loss tumors. Complete PTEN loss and PIK3CA mutations were not mutually exclusive, with PIK3CA mutation rate of 24% and 14% in PTEN loss and intact, respectively (p=0.3). There was no association of PTEN loss with KRAS mutations (p=0.3), although there were non-significant trends toward higher rates of CIMP-High, BRAF mutations, and R-sided tumors (OR 3.2, 2.7, and 1.6, respectively; p<0.2), consistent with an association with the serrated adenoma pathway and epigenetic inactivation. In the TCGA, PTEN protein loss (defined by the lowest 12% of expression) was associated with increased AKT signaling (77% increase in pAKT/AKT, p<0.01) and a similar trend with CIMP-H tumors (OR 3.1, p=0.13). Conclusions: In patient samples, PTEN loss is independent of KRAS and PIK3CA mutations, associated with robust AKT pathway activation, and may be more prominent in tumors with hypermethylation and BRAF mutations.

Evaluation of Hepatic-Metastasis Risk of Colorectal Cancer upon the Protein Signature of PI3K/AKT Pathway

2008 ◽  
Vol 7 (8) ◽  
pp. 3507-3515 ◽  
Author(s):  
Bin Kang ◽  
Chunyi Hao ◽  
Hongyi Wang ◽  
Jun Zhang ◽  
Rui Xing ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Hepatic Metastasis ◽  
Akt Pathway ◽  
Protein Signature
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