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Wingless-type MMTV integration site family, member 16
Symbol WNT16
External IDs OMIM606267 MGI2136018 HomoloGene62175 GeneCards: WNT16 Gene
RNA expression pattern
PBB GE WNT16 221113 s at tn.png
More reference expression data
Species Human Mouse
Entrez 51384 93735
Ensembl ENSG00000002745 ENSMUSG00000029671
UniProt Q9UBV4 Q9QYS1
RefSeq (mRNA) NM_016087 NM_053116
RefSeq (protein) NP_057171 NP_444346
Location (UCSC) Chr 7:
120.97 – 120.98 Mb
Chr 6:
22.29 – 22.3 Mb
PubMed search [1] [2]

Protein Wnt-16 is a protein that in humans is encoded by the WNT16 gene.[1][2] It has been proposed that stimulation of WNT16 expression in nearby normal cells is responsible for the development of chemotherapy-resistance in cancer cells.[3]

The WNT gene family consists of structurally related genes that encode secreted signaling proteins. These proteins have been implicated in oncogenesis and in several developmental processes, including regulation of cell fate and patterning during embryogenesis. This gene is a member of the WNT gene family. It contains two transcript variants diverging at the 5' termini. These two variants are proposed to be the products of separate promoters and not to be splice variants from a single promoter. They are differentially expressed in normal tissues, one of which (variant 2) is expressed at significant levels only in the pancreas, whereas another one (variant 1) is expressed more ubiquitously with highest levels in adult kidney, placenta, brain, heart, and spleen.[2]

WNT16B expression is regulated by nuclear factor of κ light polypeptide gene enhancer in B cells 1 (NF-κB) after DNA damage, as can occur to normal cels during radiation or chemotherapy. Subsequently WNT16B signals in a paracrine manner to activate the Wnt expression program in tumor cells. The expression of WNT16B in the tumor microenvironment attenuates the effects of cytotoxic chemotherapy in vivo, promoting tumor cell survival and disease progression. This implies a mechanism by which cycles of genotoxic therapy might enhance subsequent treatment resistance in the tumor microenvironment.[3]


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