COL10A1-DDR2 axis promotes the progression of pancreatic cancer by regulating MEK/ERK signal transduction.
COL10A1-DDR2 axis promotes the progression of pancreatic cancer by regulating MEK/ERK signal transduction.
复制标题
DOI:
10.3389/fonc.2022.1049345
复制
发表时间:
2022
影响因子:
4.7
通讯作者:
Zhang, Qingling
中科院分区:
文献类型:
--
作者:
Wen, Zhihui;Sun, Jingbo;Luo, Junjie;Fu, Yun;Qiu, Yue;Li, Yanyan;Xu, Yangwei;Wu, Hongmei;Zhang, Qingling
Pancreatic ductal adenocarcinoma (PDAC) is one of the most lethal malignant tumors with a poor prognosis. Type X collagen α 1 chain (COL10A1), a member of the collagen family, is a gene associated with the progression of a variety of human tumors, but the specific function and molecular mechanism of COL10A1 in pancreatic cancer remain unclear. Our study found that COL10A1 is highly expressed in pancreatic cancer cells and tissues, and its high expression is related to poor prognosis and some clinicopathological features, such as tumor size and differentiation. Biological functional experiments showed that overexpression of COL10A1 enhanced the proliferation and migration of PDAC cells. Interestingly, discoid protein domain receptor 2 (DDR2), the receptor of COL10A1, is regulated by COL10A1. We found that the COL10A1-DDR2 axis activates the mitogen-activated protein kinase (MEK)/extracellular signal-regulated kinase (ERK) pathway, which leads to epithelial-mesenchymal transformation (EMT) and accelerates the progression of pancreatic cancer. In summary, COL10A1 regulates PDAC cell proliferation and MEK/ERK signaling pathways by binding to DDR2 to promote migration, invasion and EMT. Our study suggested that COL10A1 might be a critical factor in promoting PDAC progression. More research is needed to confirm COL10A1 as a potential biomarker and therapeutic target for PDAC.
登录
查看更多内容
DOI:
10.1016/b978-0-12-800180-6.00002-5
发表时间:
2014
影响因子:
--
作者:
Leitinger, Birgit
通讯作者:
Leitinger, Birgit
影响因子:
4
作者:
Huang H;Li T;Ye G;Zhao L;Zhang Z;Mo D;Wang Y;Zhang C;Deng H;Li G;Liu H
通讯作者:
Liu H
影响因子:
17.1
作者:
Coghlan RF;Oberdorf JA;Sienko S;Aiona MD;Boston BA;Connelly KJ;Bahney C;LaRouche J;Almubarak SM;Coleman DT;Girkontaite I;von der Mark K;Lunstrum GP;Horton WA
通讯作者:
Horton WA
DOI:
10.1016/j.bbapap.2012.10.014
发表时间:
2013-10
影响因子:
3.2
作者:
Carafoli, Federico;Hohenester, Erhard
通讯作者:
Hohenester, Erhard
影响因子:
28.2
作者:
Hammerman PS;Sos ML;Ramos AH;Xu C;Dutt A;Zhou W;Brace LE;Woods BA;Lin W;Zhang J;Deng X;Lim SM;Heynck S;Peifer M;Simard JR;Lawrence MS;Onofrio RC;Salvesen HB;Seidel D;Zander T;Heuckmann JM;Soltermann A;Moch H;Koker M;Leenders F;Gabler F;Querings S;Ansén S;Brambilla E;Brambilla C;Lorimier P;Brustugun OT;Helland A;Petersen I;Clement JH;Groen H;Timens W;Sietsma H;Stoelben E;Wolf J;Beer DG;Tsao MS;Hanna M;Hatton C;Eck MJ;Janne PA;Johnson BE;Winckler W;Greulich H;Bass AJ;Cho J;Rauh D;Gray NS;Wong KK;Haura EB;Thomas RK;Meyerson M
通讯作者:
Meyerson M