Oncotarget


A novel curcumin analog inhibits canonical and non-canonical functions of telomerase through STAT3 and NF-κB inactivation in colorectal cancer cells


FOR IMMEDIATE RELEASE
2019-10-24

The cover for issue 44 of Oncotarget features Figure 10, "Schematic representation of compound 19 in colorectal cancer cells," by Chung, et al.

However, it is not well-understood the molecular mechanism of curcumin for the cancer stem cells and telomerase in colorectal cancer.

In this study, compound 19, a nitrogen-containing curcumin analog, was used to treat human colorectal cancer cells.

Compound 19 exerted anti-inflammatory activities by deactivating STAT3 and NF-κB. In cancer stem cell populations, CD44, Oct-4 and ALDHA1 expressions were abolished upon treating with compound 19.

Figure 10: Schematic representation of compound 19 in colorectal cancer cells. Compound 19 concurrently inhibits STAT3 and NF-?B transcription factors in colorectal cancer. Both STAT3 and NF-?B transcriptionally activate self-renewal genes and telomerase that resulted in enhanced stemness. Compound 19 also arrested cell cycle and induced apoptosis in the caspase-3 activated pathway. Our model suggests that a novel curcumin analog efficiently inhibits cancer stemness by deactivating STAT3 and NF-?B, and consequently decreasing telomerase activity and downregulating self-renewal gene expressions.

Dr. Seyung S. Chung and Dr. Jaydutt Vadgama said, "Colorectal cancer (CRC) is the third leading mortality in the United States and fourth leading cause of cancer-related death globally."

Therefore, we tested a nitrogen-containing novel curcumin analog, compound 19, with the potential to simultaneously inhibit cancer stemness and telomerase in human colorectal cancer cells.

We herein demonstrate the novel curcumin analog that inhibits cancer stem cell phenotype and telomerase in colorectal cancer cells.

Cancer stem cells are unique cell populations that can differentiate and generate cancer cells in various types of cancer including colorectal cancer.

This non-canonical function of telomerase attracted more attention to target telomerase for concurrently inhibiting cancer stem cell phenotype and telomerase in colorectal cancer therapeutic approaches.

We report a novel synthetic curcumin analogs inhibition on cancer stem cell phenotype and telomerase activity by inactivation of STAT3 and NF-κB in colorectal cancer stem cells.

The Chung/Vadgama research team concluded, "The novel curcumin analog inhibits cancer stem cell phenotype in colon cancer cells."

Full text - https://doi.org/10.18632/oncotarget.27000

Correspondence to - Seyung S. Chung - [email protected] and Jaydutt Vadgama - [email protected]

Keywords - curcumin analog, cancer stem cells, colorectal cancer, STAT3, NF-κB



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