Researchers have found a new genetic link to the development of metastatic cervical cancer. This article discusses how the overexpression of the gene AAC-11 leads to the production of other proteins that induce anti-apoptosis effects in the cell. The researchers found that levels of expression of AAC-11 were low in normal cervical tissue as well as cervical tissue that is in the early stages of becoming cancerous. The levels of AAC-11 increased by 200 to 400% in cervical cancer that had invaded regional lymph nodes or became metastatic (1). This indicates that AAC-11 is not the primary mutation that leads to the development of cervical cancer; rather, it is a mutation that occurs after the cancer develops but aids the progression by inhibiting apoptosis.
The Raw Data
The over-expression of AAC-11 clearly leads to increased MMP levels as well as decreased TIMP levels. Together, these 2 events could lead to resistance to apoptosis because the cell would no longer receive extra-cellular signals which would tell it to either undergo apoptosis or stop proliferation. I find it interesting that AAC-11 was expressed at normal levels in the primary stages of cancer, because I would think that the cell would need to resist apoptosis signals throughout the entire pathway to becoming cancerous. However, I do believe that the protein products of this gene would be viable targets for drugs that would be designed to inhibit that metastasis of already confirmed cervical cancer.
1. Kim, Jin Woo, Hyun Suk Cho, Jeong Hyun Kim, Soo Young Hur, Tae Eung Kim,
Joon Mo Lee, In-Kyung Kim, and Sung Eun Namkoong. "AAC-11
Overexpression Induces Invasion and Protects Cervical Cancer Cells from
Apoptosis." Laboratory Investigation (n.d.): n. pag. Web. 3 June 2014.
2. Nagase, Hideaki, Robert Visse, and Gillian Murphy. "Structure and Function of Matirix Metalloproteinases and TIMPs." Cardiovascular Research (2006): n. pag. Web