Disease relevance of WNT10B

• We next investigated expression of WNT10B in human gastric cancer [1].
• These findings suggest that the WNT10B gene may be involved in human breast cancer, and show that there is differential expression of the WNT10B gene in benign and malignant disease [2].
• A novel human Wnt gene, WNT10B, maps to 12q13 and is expressed in human breast carcinomas [2].
• WNT10B mRNA was expressed in the majority of squamous cell carcinoma cell lines derived from esophageal cancer and cervical cancer [3].
• WNT10B mRNA was relatively highly expressed in TE3, TE6, TE10, TE11 (esophageal cancer), Hs700T (pancreatic cancer), SKG-IIIa, HeLa S3 (cervical cancer), and T-47D (breast cancer) [3].

High impact information on WNT10B

• The WNT10B gene was also expressed in some cancer and non cancerous breast cell lines [2].
• Membrane-type 1 matrix metalloproteinse (MT1MMP) was upregulated by WNT10B and activation of WNT signaling [4].
• MT1MMP immunolocalized to cells identical to WNT10B and beta-catenin staining [4].
• WNT10B was most homologous to WNT10A (64.5% total amino-acid identity) among human WNTs [1].
• WNT10B and WNT1 genes were also clustered in human chromosome 12q13 region [5].

Chemical compound and disease context of WNT10B

• Elevated levels of estrogen and heightened expression of the WNT10B proto-oncogene have been implicated in the development of human malignant breast tumors because they enhance the proliferation of mammary tissue [6].

Biological context of WNT10B

• Proto-oncogene WNT10B is up-regulated by tumor necrosis factor alpha in human gastric cancer cell line MKN45 [1].
• Here, we cloned and characterized human WNT10B, which showed Gly60Asp amino-acid substitution compared with human WNT10B previously reported by another group [1].
• Gly60 WNT10B allele was identified in 2 human genome draft sequences and 7 human ESTs, while Asp60 WNT10B allele was not identified in any human genome draft sequences or ESTs [1].
• Expression and regulation of WNT10B in human cancer: up-regulation of WNT10B in MCF-7 cells by beta-estradiol and down-regulation of WNT10B in NT2 cells by retinoic acid [3].

Anatomical context of WNT10B

• The expression pattern of WNT10B reveals that it is synthesized in many adult tissues with the highest levels found in heart and skeletal muscle [7].
• WNT10B might be implicated in self renewal of stem cells as well as in carcinogenesis through activation of the WNT - beta-catenin pathway [3].
• To investigate if estrogen and these four pyrethroid insecticides could affect the expression of a gene related to mammary gland development, WNT10B expression in pyrethroid-treated MCF-7 cells was examined [6].

Associations of WNT10B with chemical compounds

• Expression of WNT10B mRNA was up-regulated by beta-estradiol in MCF-7 cells expressing estrogen receptors [3].
• Expression of WNT10B mRNA was down-regulated by all-trans retinoic acid in NT2 cells with the potential of self renewal and neuronal differentiation [3].
• The non-estrogenic pyrethroids, d-trans allethrin and permethrin, demonstrated a similar elevation of WNT10B expression at a lower concentration, but not at the higher concentration [6].
• When compared to the solvent-treated controls, sumithrin, fenvalerate and estrogen treated MCF-7 cells all had increased levels of WNT10B expression [6].

Regulatory relationships of WNT10B

• Moreover, we show here that SMYD3 could promote breast carcinogenesis by directly regulating expression of the proto-oncogene WNT10B [8].

Analytical, diagnostic and therapeutic context of WNT10B

• In normal and benign proliferations of human breast tissue, WNT10B expression was not detected by ribonuclease protection assays but was found at low levels in RT-PCR experiments [2].
• Southern blot analysis of the carcinoma expressing the highest levels of WNT10B showed no amplification or rearrangement of the gene [2].
• WNT10B was localized to 12q13.1 by PCR typing of a human/rodent monochromosomal panel and fluorescent in situ hybridization [7].
• Reverse-transcriptase polymerase chain reaction (RT-PCR), nested PCR and Southern hybridization were employed to detect WNT10B expression [6].

References