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. 2020 Apr 17;5:47. doi: 10.1038/s41392-020-0147-5

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© The Author(s) 2020

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 1 — PSAT1 was regulated by G9A and enhanced cell proliferation in colorectal cancer. a Relative expression of PSAT1 in normal and tumor tissues from colon cancer and rectal cancer samples from the TCGA database (FC (PSAT1 in colon cancer) = 2.02; FC (PSAT1 in rectal cancer) = 2.06; ****p < 0.0001; cancer versus normal). b PSAT1 expression between CRC tissue specimens and the corresponding normal specimens was examined by western blot assay (n = 12 pairs; N normal, T tumor). c Representative immunohistochemical images and semiquantitative analysis of PSAT1 protein between CRC tissue specimens and the corresponding normal tissues in the tissue chip (immunohistochemical staining, scale bar = 100 µm, n = 30 pairs, *p < 0.05). d Colony formation assay of HCT116 and DLD-1 cells (stably expressing PSAT1 shRNA) in soft agar for 14 days. e Xenograft tumor volumes were determined in nude mice after generation of tumors using HCT116 and DLD-1 cells stably expressing NTC or PSAT1 shRNA. (n = 5, *p < 0.05, **p < 0.01). f Relative expression of G9A in the normal and cancer samples of CRC from the TCGA database. The fold changes (FCs) of G9A expression in colon and rectal cancer were 1.26 and 1.37, respectively (****p < 0.0001; cancer versus normal). g Representative immunohistochemical images and semiquantitative analysis of G9A protein between CRC tissue specimens and the corresponding normal specimens in the tissue chip immunohistochemical staining; scale bar = 100 µm; n = 30 pairs; *p < 0.05). h, i After depletion of G9A, the protein expression of G9A and related metabolic enzymes in HCT116 and DLD-1 cells was investigated by western blot assay. j Xenograft tumor volumes were determined in nude mice after generation of tumors using HCT116 and DLD-1 cells stably expressing NTC or G9A shRNA (n = 5, *p < 0.05). k NTC or G9A siRNA was transfected into DLD-1 and HCT116 cells or BIX (BIX01294, 5 μM) was added to DLD-1 and HCT116 cells for 48 h. H3K9me1 and H3K9me2 levels in the PSAT1 promoter were analyzed by ChIP assay. l Cell cycle analyses were carried out in HCT116 and DLD-1 cells expressing NTC or PSAT1 siRNA by flow cytometry. m The protein expression levels of total mTOR, p-mTOR, total P70S6K, p-P70S6K, and cyclin D1 were examined by western blot in HCT116 and DLD-1 cells expressing NTC or PSAT1 siRNA. n A model of the possible mechanism underlying PSAT1 regulation of cancer development in CRC