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. 2018 Jun;15(6):9641-9646.
doi: 10.3892/ol.2018.8580. Epub 2018 Apr 26.

Cardamonin reduces chemotherapy resistance of colon cancer cells via the TSP50/NF-κB pathway in vitro

Affiliations

Cardamonin reduces chemotherapy resistance of colon cancer cells via the TSP50/NF-κB pathway in vitro

Sen Lu et al. Oncol Lett. 2018 Jun.

Abstract

It has previously been reported that cardamonin is able to regulate glycometabolism and vasodilation whilst also exhibiting anti-inflammatory and antitumor properties. The antitumor effect of cardamonin is multifaceted, and so it is necessary to investigate the antitumor mechanisms of cardamonin at the molecular level. Cardamonin alters chemotherapy-resistant colon cancer cell growth; however, the underlying mechanism is unknown. The present study was conducted to investigate the effect of cardamonin on chemotherapy-resistant colon cancer cells and the possible mechanisms of action. Cardamonin significantly suppressed the growth of chemotherapy-resistant colon cancer cells, induced apoptosis and promoted caspase-3/9 activity and Bax protein expression in 5-fluorouracil (5-FU)-resistant HCT-116 cells. Cardamonin significantly suppressed c-MYC, octamer-binding transcription factor 4, cyclin E, testes-specific protease 50 and nuclear factor-κB protein expression in 5-FU-resistant HCT-116 cells. The findings of the present study demonstrate that cardamonin suppresses chemotherapy-colon cancer cell via the NF-κB pathway in vitro.

Keywords: cardamonin; chemotherapy-colon cancer cell; nuclear factor-κB.

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Figures

Figure 1.
Figure 1.
Chemical structure of cardamonin.
Figure 2.
Figure 2.
Effect of cardamonin on chemotherapy-resistant colon cancer cell growth. **P<0.01 vs. DMSO control group. DMSO, dimethyl sulfoxide.
Figure 3.
Figure 3.
Effect of cardamonin on chemotherapy-resistant colon cancer apoptosis. Effect of cardamonin on chemotherapy-resistant colon cancer apoptosis rate using (A) statistical analysis, and (B) flow cytometer. **P<0.01 vs. DMSO control group. DMSO, dimethyl sulfoxide.
Figure 4.
Figure 4.
Effect of cardamonin on (A) caspase-3 and (B) caspase-9 activity in chemotherapy-resistant colon cancer cells. **P<0.01 vs. DMSO control group. DMSO, dimethyl sulfoxide.
Figure 5.
Figure 5.
(A) Western blotting and densitometry analysis of the effect of cardamonin on (B) Bax, (C) c-MYC and (D) Oct4 protein expression in 5-fluorouracil-resistant colon cancer cells. **P<0.01 vs. DMSO control group. Bax, Bcl-2-associated X protein; c-MYC, Myc proto-oncogene protein; Oct4, octamer-binding transcription factor 4; DMSO, dimethyl sulfoxide.
Figure 6.
Figure 6.
(A) Western blotting and densitometry analysis of the effect of cardamonin on (B) cyclin E, (C) TSP50 and (D) NF-κB protein expression in 5-fluorouracil-resistant colon cancer cells. **P<0.01 vs. DMSO control group. TSP50, testes-specific protease 50; NF-κB, nuclear factor-κB; DMSO, dimethyl sulfoxide.
Figure 7.
Figure 7.
Cardamonin suppresses chemotherapy-resistance in colon cancer cells via the TSP50/NF-κB pathway in vitro. TSP50, testes-specific protease 50; NF-κB, nuclear factor-κB; Bax, Bcl-2-associated X protein; c-MYC, Myc proto-oncogene protein.

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