Researchers discovered the carcinogenic nature of ZNF703 in 2011 while conducting research on the classification and resistance of various oncogenes.^[5] Researchers attempted to discern factors associated with various cancer types through observation of the oncogenic mechanism on a molecular scale.^[5] The luminal B cancer pathway exhibited an amplification of 5 different genomic areas including the chromosome region 8p12.^[5] Amplification of region 8p12 occurred through transcriptional regulation of ZNF703.^[5]

ZNF703 is located on human chromosome 8 at the short arm region commonly named chromosome region 8p12.^[2] Tumors generated by ZNF703 have shown loss in size beginning at the telomere and ending at 8p12 while the 8p12-11 region has increased size.^[10] A fluctuation between increase and decrease is present along the 8p12-8p21 boundary region of the chromosome.^[10] A pattern has been found that involves three similar regions of disrupted growth and four regions of enhanced growth starting from the telomere and ending at the centromere.^[10]

The ZNF703 gene generally plays an active role in luminal B tumor cells contained in mammary ducts.^[2] Typically, ZNF703 expression is greater when the tumors are estrogen receptor positive as opposed to estrogen receptor negative.^[2] ZNF703 is co-expressed in a nuclear complex containing genes DCAF7, NCRO2 and PHB2.^[2] ZNF703 generates a nuclear protein responsible for oestrogen receptor associated protein repression.^[2] Gene expression of stem cells are triggered when the ZNF703 gene becomes overexpressed in the complex.^[2] As a result, both regular cells and cancer stem cell abundance increases rapidly.^[2] ZNF703 overexpression also causes primary and secondary tumorsphere development alongside amplified production of CD49F- positive cells associated with colon cancer.^[2]

ZNF703 also experiences target regulation of cancer cells through the transcription of RNA SPRY4-It1.^[11] RNA SPRY4-IT1 is a non-coding gene responsible for preventing apoptosis and generating large tumors.^[11]

Researchers recently established a link between the trigger gene ZNF703 and Akt/mTOR pathway activation involved in the cellular cycle resulting in lung tumor formation.^[12]

The lifespan of individuals with colorectal cancer and luminal cancer have different prognosis depending on the amount of expression of the ZNF703 gene.^[8] Low amounts of transcription of ZNF703 usually leads to a healthier prognosis than individuals experiencing higher levels of transcription of the oncogene.^[8] ZNF703 is a target for therapeutic medicines since survival rates increase as transcription rates decrease.^[8]

The drug Tamoxifen is a commonly administered drug used to treat luminal cancers in patients.^[9] Half of patients treated with Tamoxifen are resistant to the drug.^[9] Overexpression of ZNF703 has been linked to Tamoxifen resistance.^[9] As transcription of the ZNF703 gene reaches substantial levels, instead of blocking cell proliferation, Tamoxifen is found to increase cancer cell division.^[9] Tamoxifen can only be given at low dosages and patients are monitored daily in order to avoid tumor growth.^[9]