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. 2021 Sep 14;10(9):1459. doi: 10.3390/antiox10091459

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© 2021 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).

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DiHEP-DPA affects the EMT process and stemness of colorectal cancer cells through modulation of TAM pola ization. (A) Decreased tumorspheres-formation efficiency (TFE) by TCCM-DPA treatment. Tumorspheres derived from HT29 and HCT116 cells were cultured for 7 d in the presence of TCCM, TCCM-DPA, or DMSO. (B) Migration of HT29 and HCT116 cells treated with TCCM or TCCM-DPA (RPMI-1640/0.5% FBS), determined by scratch assay. Scale bar: 100 μm. (C) Cell migration (without Matrigel) and invasion (with Matrigel) of HT29 and HCT116 cells exposed to TCCM or TCCM-DPA, determined by Transwell assays. Scale bar: 100 μm. (D) Transcript levels of the EMT markers, E-cadherin, N-cadherin, Vimentin in TCCM-treated HT29, and HCT116 cells, determined using gene-specific primers and quantitative RT-PCR. β-actin was detected as an internal reference. (E,F) Expression of EMT protein markers and cancer stemness markers (CD133, CD44, and Sox2), determined by Western blotting using the corresponding antibodies. (G) Decrease in the ALDH-positive cell population by treatment with TCCM-DPA. Colorectal cancer cells were treated with TCCM or TCCM-DPA for 48 h and analyzed by FACS. Data from triplicate experiments are presented as the means ± SD (^# p < 0.05 versus the DMSO-treated control group; * p < 0.05 versus the TCCM group).

DiHEP-DPA affects the EMT process and stemness of colorectal cancer cells through modulation of TAM pola ization. (A) Decreased tumorspheres-formation efficiency (TFE) by TCCM-DPA treatment. Tumorspheres derived from HT29 and HCT116 cells were cultured for 7 d in the presence of TCCM, TCCM-DPA, or DMSO. (B) Migration of HT29 and HCT116 cells treated with TCCM or TCCM-DPA (RPMI-1640/0.5% FBS), determined by scratch assay. Scale bar: 100 μm. (C) Cell migration (without Matrigel) and invasion (with Matrigel) of HT29 and HCT116 cells exposed to TCCM or TCCM-DPA, determined by Transwell assays. Scale bar: 100 μm. (D) Transcript levels of the EMT markers, E-cadherin, N-cadherin, Vimentin in TCCM-treated HT29, and HCT116 cells, determined using gene-specific primers and quantitative RT-PCR. β-actin was detected as an internal reference. (E,F) Expression of EMT protein markers and cancer stemness markers (CD133, CD44, and Sox2), determined by Western blotting using the corresponding antibodies. (G) Decrease in the ALDH-positive cell population by treatment with TCCM-DPA. Colorectal cancer cells were treated with TCCM or TCCM-DPA for 48 h and analyzed by FACS. Data from triplicate experiments are presented as the means ± SD (^# p < 0.05 versus the DMSO-treated control group; * p < 0.05 versus the TCCM group).