OLR1 Promotes Invasion and Metastasis of Pancreatic Cancer by Regulating the Expression of HMGA2 through c-Myc

Yang, Gang; Zhao, Fangyu; Qiu, Jiangdong; Liu, Yueze; Zhang, Taiping; Zhao, Yupei

doi:10.1016/j.jamcollsurg.2019.08.1133

Cited by 1 publication

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“…Consistently, OLR1 activation plays an important role in the pathogenesis of different cancers particularly pancreatic cancer. 194 , 195 OLR1, through upregulation of c-Myc, can promote pancreatic cancer cells proliferation, metastasis, and chemoresistance to gemcitabine. OLR1 is overexpressed in pancreatic cancer.…”

Section: The Effect Of C-myc On Cancer Cells Metabolismmentioning

confidence: 99%

“…Similarly, overactivity of OLR1/c-Myc/ HMGA2 axis is associated with poor prognosis among patients with pancreatic cancer. 134 , 195 , 196 HMGA2 is a transcription factor that binds to AT-rich sequences to change the structure of chromatin. It has been implicated in tumorigenesis, EMT, and chemoresistance.…”

Section: The Effect Of C-myc On Cancer Cells Metabolismmentioning

confidence: 99%

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Target c-Myc to treat pancreatic cancer

Ala

2022

Cancer Biology & Therapy

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C-Myc overexpression is a common finding in pancreatic cancer and predicts the aggressive behavior of cancer cells. It binds to the promoter of different genes, thereby regulating their transcription. C-Myc is downstream of KRAS and interacts with several oncogenic and proliferative pathways in pancreatic cancer. C-Myc enhances aerobic glycolysis in cancer cells and regulates glutamate biosynthesis from glutamine. It provides enough energy for cancer cells’ metabolism and sufficient substrate for the synthesis of organic molecules. C-Myc overexpression is associated with chemoresistance, intra-tumor angiogenesis, epithelial-mesenchymal transition (EMT), and metastasis in pancreatic cancer. Despite its title, c-Myc is not “undruggable” and recent studies unveiled that it can be targeted, directly or indirectly. Small molecules that accelerate c-Myc ubiquitination and degradation have been effective in preclinical studies. Small molecules that hinder c-Myc-MAX heterodimerization or c-Myc/MAX/DNA complex formation can functionally inhibit c-Myc. In addition, c-Myc can be targeted through transcriptional, post-transcriptional, and translational modifications.

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Section: The Effect Of C-myc On Cancer Cells Metabolismmentioning

confidence: 99%