skin & beauty

cancer

PLA2G6

Cell Barrier Integrity & Melanoma Progression (PLA2G6)

Written by Shany Lahan, MS (Neuroscience) on January 13th, 2021

PLA2G6 promotes cell death by altering the cell barrier. How might variants of PLA2G6 increase the risk of a type of skin cancer called melanoma? Find out below.

Summary

PLA2G6 codes for a protein that promotes cell death by modulating cell barrier integrity. Variants of PLA2G6 may play a role in melanoma by altering PLA2G6 production and dysregulating cell death. Lifestyle and diet modifications may counteract the effects of these variants by limiting or balancing levels of PLA2G6.

PLA2G6 and Melanoma

The PLA2G6 gene codes for phospholipase A2 group VI (PLA2G6), an enzyme that breaks down a type of fat called a phospholipid. This releases fatty acids and other molecules that function as precursors for cellular processes [R, R].

Phospholipids are abundant in the outermost barrier of cells, or the cell membrane. The regulated breakdown of phospholipids is essential for maintaining the integrity of the cell membrane, and dysregulation of phospholipid breakdown has been suggested to promote programmed cell death (apoptosis) [R].

Apoptosis supports the immune cell-mediated removal of infected, damaged, or cancerous cells. In cancer, cells are often able to evade apoptosis and continue dividing uncontrollably [R].

Although other enzymes exist to balance the effects of PLA2G6 on the cell membrane, one study has reported that PLA2G6 specifically functions to increase the breakdown of phospholipids, thereby contributing to changes in the cell membrane that may promote apoptosis [R].

Interestingly, researchers have hypothesized that low apoptotic activity may actually be beneficial in immune cells that function to clear cancerous cells, suggesting that PLA2G6 levels must remain balanced in order to avoid unwanted effects [R].

Variants of PLA2G6 have been associated with melanoma, a type of skin cancer. These variants may alter the production of PLA2G6, resulting in loss of cell membrane integrity and consequent apoptosis [R, R, R, R].

Your PLA2G6 Results for Melanoma

SNP Table

variant	genotype	frequency	risk allele
rs2284063
rs132985

Primary SNP:

PLA2G6 rs2284063 [R, R, R]

‘A’ = Higher odds of melanoma, relative to ‘G’
‘G’ = Lower odds of melanoma, relative to ‘A’

Other Important SNPs:

PLA2G6 rs132985 [R, R]

‘C’ = Higher odds of melanoma, relative to ‘T’
‘T’ = Lower odds of melanoma, relative to ‘C’

Recommendations

Lifestyle

Maintaining a Healthy Weight

Obesity may exacerbate stimulation of apoptotic pathways [R].

In men, being obese or overweight has been associated with an increased risk of melanoma in 21 studies of almost 25,000 people [R, R, R].

Weight loss may also help improve the effectiveness of chemotherapeutic drugs for melanoma, as seen in a study in mice [R].

Maintaining a healthy weight may help prevent melanoma by limiting programmed cell death.

Reducing Alcohol Intake

Long-term alcohol intake may significantly increase apoptosis [R].

Meta-analyses of 20 studies have associated moderate alcohol consumption with a slight increase (7-18%) in the overall incidence of melanoma. A study of 1374 cases found that alcohol specifically increased the risk of melanoma in sites with low exposure to sunlight (such as the trunk) [R, R, R].

Reducing alcohol intake may help prevent melanoma by limiting programmed cell death.

Diet

Reducing Glycemic Load

High sugar consumption may suppress apoptosis and promote the survival of cancer cells [R].

The glycemic load is a measure of how much a food increases blood glucose levels without taking into account the rate at which it increases them (as the glycemic index does).

Two studies on an Italian population of over 1000 people associated the intake of high-glycemic-load foods such as refined flours, sweets, candy bars, and chocolate with an increased incidence of melanoma in women. Conversely, soluble fiber had a protective effect in a small study [R, R, R].

Reducing glycemic load may help prevent melanoma by balancing programmed cell death.

Shany Lahan

MS (Neuroscience)

Shany received her MSc in Neuroscience from Western University.

Prior to joining SelfDecode, Shany conducted research related to Alzheimer’s disease, and taught science to undergraduate students. She believes that research should be accessible to everyone, regardless of scientific background. Shany joined SelfDecode with a mission to help others optimize their health and wellbeing – as well as help them understand the science behind it all.

Disclaimer

The information on this website has not been evaluated by the Food & Drug Administration or any other official medical body. This information is presented for educational purposes only, and may not be used to diagnose or treat any illness or disease.

Also keep in mind that the “Risk Score” presented in this post is based only on a select number of SNPs, and therefore only represents a small portion of your total risk as an individual. Furthermore, these analyses are based primarily on associational studies, which do not necessarily imply causation. Finally, many other (non-genetic) factors can also play a significant role in the development of a disease or health condition — therefore, carrying any of the risk-associated genotypes discussed in this post does not necessarily mean you are at increased risk of developing a major health condition.

Always consult your doctor before acting on any information or recommendations discussed in this post — especially if you are pregnant, nursing, taking medication, or have been officially diagnosed with a medical condition.

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