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  • 1.
    Lööf, Jasmine
    et al.
    University of Skövde, School of Life Sciences. University of Skövde, The Systems Biology Research Centre.
    Pfeifer, Daniella
    Linköping University.
    Ding, Zhenyu
    Linköping University.
    Sun, Xiao-Feng
    Linköping University.
    Zhang, Hong
    University of Skövde, School of Life Sciences. University of Skövde, The Systems Biology Research Centre.
    Effects of ΔNp73β on Cisplatin Treatment in Colon Cancer Cells2012In: Molecular Carcinogenesis, ISSN 0899-1987, E-ISSN 1098-2744, Vol. 51, no 8, p. 628-635Article in journal (Refereed)
    Abstract [en]

    p73 can activate transcription of p53-responsive genes, thereby inhibiting cell growth. An alternative promoter in the TP73 gene gives rise to an N-terminally truncated isoform of p73, DNp73, which lacks the transactivation domain of the full length TAp73 protein. TAp73 is considered pro-apoptotic, and DNp73 anti-apoptotic. In this study, we overexpressed DNp73β in p53 wild type and p53 mutant colon cancer cell lines and further exposed the cells to cancer therapeutic drug cisplatin. The results showed that cisplatin decreased the protein expression levels of DNp73β in a dose-dependent manner, and both TAp73 and p53 were upregulated after cisplatin treatment. Further, clonogenic potential and cell viability were decreased, and apoptotic cells increased, in p53 mutant and in p53 wild type cells. Cellular viability was significantly higher in DNp73β-cells than mock-transfected cells. However, DNp73β overexpression did not affect the cellular susceptibility to cisplatin. In conclusion, the overexpression of DNp73β increases viability in p53 wild type and p53 mutant colon cancer cells, and cisplatin induces the degradation of DNp73β in a dose-dependent manner.

  • 2.
    Lööf, Jasmine
    et al.
    University of Skövde, The Systems Biology Research Centre. University of Skövde, School of Life Sciences.
    Rosell, Johan
    Department of Oncology, Linköping University Hospital, S-58185 Linköping, Sweden.
    Bratthäll, Charlotte
    Department of Oncology, Linköping University Hospital, S-58185 Linköping, Sweden.
    Doré, Siv
    Department of Pathology, Linköping University, Linköping, Sweden.
    Starkhammar, Hans
    Department of Oncology, Linköping University Hospital, S-58185 Linköping, Sweden.
    Zhang, Hong
    University of Skövde, The Systems Biology Research Centre. University of Skövde, School of Life Sciences.
    Sun, Xiao-Feng
    Department of Oncology, Linköping University, Linköping, Sweden.
    Impact of PINCH expression on survival in colorectal cancer patients2011In: BMC Cancer, ISSN 1471-2407, E-ISSN 1471-2407, Vol. 11, p. Artikelnr 103-Article in journal (Refereed)
    Abstract [en]

    Background: The adaptor protein PINCH is overexpressed in the stroma of several types of cancer, and is an independent prognostic marker in colorectal cancer. In this study we further investigate the relationship of PINCH and survival regarding the response to chemotherapy in colorectal cancer. Results: Paraffin-embedded tissue sections from 251 primary adenocarcinomas, 149 samples of adjacent normal mucosa, 57 samples of distant normal mucosa and 75 lymph node metastases were used for immunohistochemical staining. Stromal staining for PINCH increased from normal mucosa to primary tumour to metastasis. Strong staining in adjacent normal mucosa was related to worse survival independently of sex, age, tumour location, differentiation and stage (p = 0.044, HR, 1.60, 95% Cl, 1.01-2.52). PINCH staining at the invasive margin tended to be related to survival (p = 0.051). In poorly differentiated tumours PINCH staining at the invasive margin was related to survival independently of sex, age and stage (p = 0.013, HR, 1.90, 95% Cl, 1.14-3.16), while in better differentiated tumours it was not. In patients with weak staining, adjuvant chemotherapy was related to survival (p = 0.010, 0.013 and 0.013 in entire tumour area, invasive margin and inner tumour area, respectively), but not in patients with strong staining. However, in the multivariate analysis no such relationship was seen. Conclusions: PINCH staining in normal adjacent mucosa was related to survival. Further, PINCH staining at the tumour invasive margin was related to survival in poorly differentiated tumours but not in better differentiated tumours, indicating that the impact of PINCH on prognosis was dependent on differentiation status.

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