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A team led by scientists at Baylor College of Medicine uncovered new evidence supporting a cancer-promoting role for enzyme MAPK6. The study, published in the journal Science Advances, shows that MAPK6 furthers cancer growth by activating the AKT pathway, a known cancer-promoting cellular mechanism. The findings suggest that therapies directed at interfering with MAPK6 activity in cancer may offer an effective treatment approach for this condition.

Yang and his colleagues began by investigating the effect of overexpressing the MAPK6 gene in normal human prostate or breast epithelial cells grown in the lab.

"We found that overexpressing MAPK6 can transform normal cells into tumor-like cells," said Yang, a member of Baylor's Dan L Duncan Comprehensive Cancer Center. "In addition, enhancing MAPK6 expression in prostate, ovarian, breast and non-small cell lung cancer cell lines that already had low to high levels of MAPK6 further promoted growth of all tumor cell lines."

These findings suggested that eliminating MAPK6 from tumor cells could reduce tumor growth. Indeed, genetically knocking down MAPK6 significantly reduced the growth of several types of cancer cells in the lab.

The researchers then investigated the mechanism mediating MAPK6 cancer-promoting activity.

"We had previously found that MAPK4, which is closely related to MAPK6, promotes cancer growth by activating the AKT pathway," Yang said. "Here, we discovered that MAPK6 also activates AKT to promote cancer growth. Both MAPK4 and MAPK6 add a phosphate group to AKT, a process called phosphorylation, but MAPK6 phosphorylates a different location in AKT than does MAPK4, and this is essential for the tumor-promoting activity of MAPK6."

 

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