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  • 1.
    Farkas, Sanja A.
    et al.
    Örebro universitet, Institutionen för hälsovetenskap och medicin.
    Befekadu, Rahel
    Örebro universitet, Institutionen för hälsovetenskap och medicin.
    Hahn-Strömberg, Victoria
    Örebro universitet, Institutionen för hälsovetenskap och medicin.
    Nilsson, Torbjörn K.
    Department of Medical Biosciences, Clinical Chemistry, Umeå University, Umeå, Sweden.
    DNA methylation and expression of the folate transporter genes in colorectal cancer2015Ingår i: Tumor Biology, ISSN 1010-4283, E-ISSN 1423-0380, Vol. 36, nr 7, s. 5581-5590Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Folate has a central role in the cell metabolism. This study aims to explore the DNA methylation pattern of the folate transporter genes FOLR1, PCFT, and RFC1 as well as the corresponding protein expressions in colorectal cancer (CRC) tissue and adjacent non-cancerous mucosa (ANCM). Our results showed statistically significant differences in the DNA-methylated fraction of all three genes at several gene regions; we identified three differentially methylated CpG sites in the FOLR1 gene, five CpG sites in the PCFT gene, and six CpG sites in the RFC1 gene. There was a pronounced expression of the FR alpha and RFC proteins in both the CRC and ANCM tissues, though the expression was attenuated in cancer compared to the paired ANCM tissues. The PCFT protein was undetectable or expressed at a very low level in both tissue types. Higher methylated fractions of the CpG sites 3-5 in the RFC1 gene were associated with a lower protein expression, suggestive of epigenetic regulation by DNA methylation of the RFC1 gene in the colorectal cancer. Our results did not show any association between the RFC and FR alpha protein expression and tumor stage, TNM classification, or tumor location. In conclusion, this is the first study to simultaneously evaluate both DNA methylation and protein expression of all three folate transporter genes, FOLR1, PCFT, and RFC1, in colorectal cancer. The results encourage further investigation into the possible prognostic implications of folate transporter expression and DNA methylation.

  • 2.
    Hahn-Strömberg, Victoria
    et al.
    Department of Medical Cell Biology, Uppsala University, Uppsala, Sweden.
    Askari, Shlear
    Department of Clinical Research, Örebro University Hospital, Örebro, Sweden.
    Ahmad, Abrar
    Department of Clinical Research, Örebro University Hospital, Örebro, Sweden.
    Befekadu, Rahel
    Örebro universitet, Institutionen för medicinska vetenskaper. Department of Clinical Research, Örebro University Hospital, Örebro, Sweden.
    Nilsson, Torbjörn K.
    Division of Clinical Chemistry, Department of Medical Biosciences, Umeå University, Umeå, Sweden.
    Expression of claudin 1, claudin 4, and claudin 7 in colorectal cancer and its relation with CLDN DNA methylation patterns2017Ingår i: Tumor Biology, ISSN 1010-4283, E-ISSN 1423-0380, Vol. 39, nr 4, artikel-id 697569Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Altered claudin expression has been described in colon, prostatic, ovarian, and breast carcinoma. However, the role of epigenetic modifications in these genes and their role in colorectal cancer is unknown. We aimed our study to investigate whether claudin protein expression and methylation of CLDN can influence the tumorigenesis of colorectal cancer. A total of 31 patients diagnosed with colorectal carcinoma was used in this study. Immunohistochemical staining was used to study protein expression in both tumor and the adjacent nonneoplastic mucosa of claudin 1, 4, and 7. To detect the DNA methylation pattern of CLDN1, 4, and 7, genomic DNA was extracted from both the tumor and the adjacent nonneoplastic mucosa. Methylation analysis was carried out using bisulfite pyrosequencing. Cell membrane staining intensity of all claudins was found significantly lower in colorectal cancer tissues when compared to paired normal mucosa (p ≤ 0.001). For claudin 4, the percentage of cells staining positively was also significantly reduced (p = 0.04). In normal mucosa, cytoplasm showed no staining for claudins in any patient, whereas in paired colorectal cancer tissues, significant cytoplasmic staining appeared both for claudin 1 (p = 0.04) and claudin 4 (p = 0.01). Tumor samples were significantly hypomethylated in CLDN1 (p < 0.05). In conclusion, our results show that CLDN1 is significantly hypomethylated in tumor samples and that the membrane staining intensity for claudin 1, 4, and 7 is significantly lower in colorectal cancer tissues than in adjacent nonneoplastic tissue. Colorectal cancer cells showed dystopic cytoplasmic location of claudins.

  • 3.
    Hedbrant, Alexander
    et al.
    Department of Health Sciences, Karlstad University, Karlstad, Sweden.
    Wijkander, Jonny
    Department of Health Sciences, Karlstad University, Karlstad, Sweden.
    Seidal, Tomas
    Department of Health Sciences, Karlstad University, Karlstad, Sweden.
    Delbro, Dick
    Örebro universitet, Institutionen för läkarutbildning.
    Erlandsson, Ann
    Department of Health Sciences, Karlstad University, Karlstad, Sweden.
    Macrophages of M1 phenotype have properties that influence lung cancer cell progression2015Ingår i: Tumor Biology, ISSN 1010-4283, E-ISSN 1423-0380, Vol. 36, nr 11, s. 8715-8725Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Stromal macrophages of different phenotypes can contribute to the expression of proteins that affects metastasis such as urokinase-type plasminogen activator (uPA), its receptor uPAR, and plasminogen activator inhibitor-1 (PAI-1), but knowledge of how essential their contribution is in comparison to the cancer cells in small cell lung cancer (SCLC) and lung squamous cell carcinoma (SCC) is lacking. The expression of uPA, uPAR, and PAI-1 and of the matrix metalloproteinases (MMP)-2 and MMP-9 were studied in human macrophages of M1 and M2 phenotype and compared to a lung SCC (NCI-H520) and a SCLC (NCI-H69) cell line. Effects of treatment with conditioned media (CM) from M1 and M2 macrophages on the expression of these genes in H520 and H69 cells as well as effects on the cell growth were investigated. In addition, data on the stromal macrophages immunoreactivity of uPAR, MMP-2, and MMP-9 in a few SCC and SCLC biopsies was included. uPAR, MMP-2, and MMP-9 were confirmed in stromal cells including macrophages in the SCC and SCLC biopsies. In vitro, both macrophage phenotypes expressed considerably higher mRNA levels of uPA, uPAR, PAI-1, and MMP-9 compared to the cancer cell lines, and regarding uPAR, the highest level was found in the M1 macrophage phenotype. Furthermore, M1 CM treatment not only induced an upregulation of PAI-1 in both H520 and H69 cells but also inhibited cell growth in both cell lines, giving M1 macrophages both tumor-promoting and tumor-killing potential.

  • 4.
    Wang, Chao-Jie
    et al.
    Dept Oncolgy, Henan Province Peoples Hospital, Zhengzhou University, Zhengzhou, Peoples R China.; Fac Hlth Sci, Div Oncol, Dept Clin & Experimental Medicine, Linköping University, Linköping, Sweden.
    Frayennbergh-Karlson, Hanna
    Fac Health Science, Div Oncology, Dept Clin & Experimental Med, Linköping University, Linköping, Sweden..
    Wang, Da-Wei
    Dept Stomatol, Hosp 1, Hebei Medical University, Shijiazhuang, Peoples R China.
    Arbman, Gunnar
    Dept Surg, Vrinnevi Hospital, Linköping University, Norrköping, Sweden.
    Zhang, Hong
    Örebro universitet, Institutionen för läkarutbildning.
    Sun, Xiao-Feng
    Fac Health Science, Div Oncology, Dept Clin & Experimental Medicine , City Council Östergötland, Linköping University, Linköping, Sweden.
    Clinicopathological significance of BTF3 expression in colorectal cancer2013Ingår i: Tumor Biology, ISSN 1010-4283, E-ISSN 1423-0380, Vol. 34, nr 4, s. 2141-2146Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Basic transcription factor 3 (BTF3) is a general RNA polymerase II transcription factor and is also involved in apoptosis regulation. Increasing evidence shows that BTF3 is aberrantly expressed in several kinds of malignancies, but there is no study to analyze BTF3 expression in colorectal cancer (CRC) patients. Applying immunohistochemistry, we detected BTF3 in CRCs (n = 156), the corresponding distant (n = 42), adjacent normal mucosa (n = 96), lymph node metastases (n = 35), and analyzed its relationships with clinicopathological and biological variables. Our results showed that BTF3 staining significantly increased from distant or adjacent normal mucosa to primary CRCs (p < 0.0001) or metastases (p = 0.002 and p < 0.0001). BTF3 was higher in distal cancers than in proximal cancers (57 % vs. 39 %, p = 0.041). It also showed stronger staining in primary CRCs stage I and II than that in stage III and IV (64 % vs. 35 %, p = 0.0004), or metastases (64 % vs. 29 %, p = 0.004). Cancers with better differentiation had a higher expression than those with worse differentiation (56 % vs. 37 %, p = 0.031). There were positive correlations of BTF3 expression with nuclear factor kappa B (NF-kappa B), RAD50, MRE11, NBS1, and AEG-1 (p < 0.05). In conclusion, BTF3 overexpression may be an early event in CRC development and could be useful biomarker for the early stage of CRCs. BTF3 has positive correlations with NF-kappa B, RAD50, MRE11, NBS1 and AEG-1, and might influence complex signal pathways in CRC.

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