O desenvolvemento de [[tumor]]es é un complexo proceso que require a [[división celular]], crecemento e supervivencia das células. Unha maneira utilizada polos tumores para regular á alza o crecemento e supervivencia das células é por medio da produción autócrina de factores de crecemento e supervivencia. A sinalización autócrina é esencial na activación do [[cancro]] e tamén para proporcionar aos tumores sinais de crecemento autosostidas.
[[Tumor]] development is a complex process that requires [[cell division]], growth, and survival. One approach used by tumors to upregulate growth and survival is through autocrine production of growth and survival factors. Autocrine signaling plays critical roles in cancer activation and also in providing self-sustaining growth signals to tumors.{{Citation needed|date=April 2013}}
===Sinalización autócrina na vía Wnt===
NormallyNormalmente, thea [[Wntvía signalingde pathwaysinalización Wnt]] leadsleva toá stabilizationestabilización ofda [[β-catenincatenina]] throughpor inactivationmedio ofda ainactivación proteindun complexcomplexo containingproteico theque tumorcontén suppressorsos supresores de tuimores [[AdenomatousPolipose adenomatosa polyposisdo colicolon|APC]] ande [[Axinaxina]]. ThisEste destructioncomplexo complexde normallydestrución triggersnormalmente β-catenindesencadea a [[phosphorylationfosforilación]] da β-catenina, inducinginducindo a itssúa degradationdegradación. De-regulation of the autocrine Wnt signaling pathway via [[mutations]] in APC and Axin have been linked to activation of various types of human [[cancer]].<ref name= "two">{{cite journal |doi=10.1016/j.ccr.2004.09.032 |title=An autocrine mechanism for constitutive Wnt pathway activation in human cancer cells |year=2004 |last1=Bafico |first1=Anna |last2=Liu |first2=Guizhong |last3=Goldin |first3=Luba |last4=Harris |first4=Violaine |last5=Aaronson |first5=Stuart A. |journal=Cancer Cell |volume=6 |issue=5 |pages=497–506 |pmid=15542433}}</ref><ref name= "three">{{cite journal |doi=10.1186/bcr1769 |title=Autocrine WNT signaling contributes to breast cancer cell proliferation via the canonical WNT pathway and EGFR transactivation |year=2007 |last1=Schlange |first1=Thomas |last2=Matsuda |first2=Yutaka |last3=Lienhard |first3=Susanne |last4=Huber |first4=Alexandre |last5=Hynes |first5=Nancy E |journal=Breast Cancer Research |volume=9 |issue=5 |pages=R63 |pmid=17897439 |pmc=2242658}}</ref> Genetic alterations that lead to de-regulation of the autocrine Wnt pathway result in transactivation of [[epidermal growth factor receptor]] (EGFR) and other pathways, in turn contributing to proliferation of tumor cells. In [[colorectal cancer]], for example, mutations in APC, axin, or β-catenin promote β-catenin stabilization and [[transcription (genetics)|transcription]] of [[genes]] encoding cancer-associated [[proteins]]. Furthermore, in human [[breast cancer]], interference with the de-regulated Wnt signaling pathway reduces proliferation and survival of cancer. These findings suggest that interference with Wnt signaling at the ligand-receptor level may improve the effectiveness of cancer therapies.<ref name= "three" />
