by Pooja Shete on  December 12, 2020 at 11:44 PM Cancer News
How Do Prostate Cancer Cells Resist Treatment?
Two genes have been identified on prostate cancer cells that become resistant to treatment. This provides a new potential target for prostate cancer treatment.

The study published in Molecular Cancer Research was conducted by Researchers at University of Georgia.

The two genes identified are ACSL3 and ACSL4 help the cancer cells to grow. According to the research conducted by Houjian Cai, associate professor in the College of Pharmacy and his colleagues, the genes function in an interconnected way.


The Centers for Disease Control (CDC) reported that prostate cancer is the second leading cause of cancer-related deaths among men in the US.

The primary therapy to treat prostate cancer is castration treatment that suppresses the male hormone which helps the cancer cells to grow. This treatment decreases the expression of ACSL3 gene.

As time passes, prostate cancer may become resistant to castration treatment. When this happens, expression of the ACSL4 gene increases.

The researchers found that when the expression of one gene becomes high, the expression of the other becomes low. The roles can also be reversed in some cases.

Cai said, "In the early stage of cancer, ACSL3 is high and ACSL4 is low. With castration treatment, expression of the ACSL3 gene becomes low, but ACSL4 becomes high. In order to treat the cancer cells effectively, you have to somehow simultaneously target the pathway driven by these two genes."

The researchers studied the function of ACSL4 using cancer cell lines that were resistant to castration treatment. Using a mouse model, the researchers inhibited ACSL4 expression to see how the tumor would response.

The researchers found that by inhibiting the ACSL4 gene expression, the cancer cells were suppressed.

Cai said, "Identifying the ACSL4 gene as a target for castration treatment-resistant prostate cancer is the first step. The next step is to find a drug that will inhibit the gene."

Source: Medindia

Most Popular on Medindia