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  • 1.
    Hussain, Showket
    et al.
    Division of Molecular Genetics & Biochemistry, Institute of Cytology & Preventive Oncology (ICMR), Noida, India.
    Singh, Neha
    Department of Biotechnology, Panjab University, Chandigarh, India.
    Salam, Irfana
    Department of Clinical Biochemistry, Sher-I-Kashmir Institute of Medical Sciences, Soura, Srinagar, Jammu and Kashmir, India.
    Bandil, Kapil
    Division of Molecular Genetics & Biochemistry, Institute of Cytology & Preventive Oncology (ICMR), Noida, India.
    Yuvaraj, M
    Division of Molecular Genetics & Biochemistry, Institute of Cytology & Preventive Oncology (ICMR), Noida, India.
    Akbar Bhat, Mohammad
    Department of Cardiovascular Thoracic Surgery, Sher-I-Kashmir Institute of Medical Sciences, Soura, Srinagar, Jammu and Kashmir, India.
    Muzaffar Mir, Mohammad
    Department of Biotechnology, Panjab University, Chandigarh, India.
    Siddiqi, Mushtaq A.
    Department of Cardiovascular Thoracic Surgery, Sher-I-Kashmir Institute of Medical Sciences, Soura, Srinagar, Jammu and Kashmir, India.
    Sobti, Ranbir C.
    Department of Biotechnology, Panjab University, Chandigarh, India.
    Bharadwaj, Mausumi
    Division of Molecular Genetics & Biochemistry, Institute of Cytology & Preventive Oncology (ICMR), Noida, India.
    Das, Bhudev C.
    Dr. B.R. Ambedkar Centre for Biomedical Research (ACBR) University of Delhi (North Campus), Delhi, India.
    Methylation-mediated gene silencing of suppressor of cytokine signaling-1 (SOCS-1) gene in esophageal squamous cell carcinoma patients of Kashmir valley2011In: Journal of Receptor and Signal Transduction Research, ISSN 1079-9893, E-ISSN 1532-4281, Vol. 31, no 2, p. 147-56Article in journal (Refereed)
    Abstract [en]

    CONTEXT: Esophageal squamous cell carcinoma (ESCC) is a leading cause of cancer-related deaths in Jammu and Kashmir. The negative regulation of tumor suppressor gene leading to change in signaling pathway is one of the major mechanisms responsible for tumorigenic transformation.

    OBJECTIVE: In the present study, the role of silencing of suppressor of cytokine signaling-1 (SOCS-1) gene, a negative regulator of JAK/STAT pathway, was analyzed in ESCC.

    METHODS: The expression pattern of SOCS-1 gene was analyzed in esophageal tumor biopsies although normal adjacent tissues that served as controls. Reverse transcriptase polymerase chain reaction (RT-PCR), immunohistochemistry, methylation-specific PCR (MSP), and human papillomavirus (HPV) detection were performed to assess the expression pattern and promoter methylation of SOCS-1 gene including HPV status in a total of 75 surgically resected tissue specimens.

    RESULTS: Compared with the level of SOCS-1 expression in normal tissues, 53% (40/75) of the tumor tissues expressed either undetectable or reduced SOCS-1 expression (>50% loss of expression), which was significantly associated with advanced clinical stage or severe histopathological grade of the disease (P < 0.01). Aberrant promoter methylation of the SOCS-1 gene was found in 45% (34/75) of the esophageal tumor tissues, which was also found to be significantly associated with advanced stage of esophageal carcinoma (P < 0.01). The prevalence of HPV infection was found in 19% of tumor cases, whereas no HPV could be detected in any of the normal adjacent tissues.

    CONCLUSION: Transcriptional inactivation of SOCS-1 gene, primarily due to its promoter hypermethylation although HPV infection, may play an important role in esophageal carcinogenesis in Kashmir.

  • 2.
    Singh, Neha
    et al.
    Department of Biotechnology, Panjab University, Chandigarh, India.
    Hussain, Showket
    Division of Molecular Genetics and Biochemistry, Institute of Cytology and Preventive Oncology (ICMR), Noida, India.
    Bharadwaj, Mausumi
    Division of Molecular Genetics and Biochemistry, Institute of Cytology and Preventive Oncology (ICMR), Noida, India.
    Kakkar, Nandita
    Department of Urology, Post Graduate Institute of Medical Education and Research, Chandigarh, India.
    Singh, S. K.
    Department of Histopathology, Post Graduate Institute of Medical Education and Research, Chandigarh, India.
    Sobti, Ranbir C.
    Department of Biotechnology, Panjab University, Chandigarh, India.
    Overexpression of signal transducer and activator of transcription (STAT-3 and STAT-5) transcription factors and alteration of suppressor of cytokine signaling (SOCS-1) protein in prostate cancer2012In: Journal of Receptor and Signal Transduction Research, ISSN 1079-9893, E-ISSN 1532-4281, Vol. 32, no 6, p. 321-7Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Prostate cancer is a leading cause of mortality in men worldwide especially in developing countries like India. The molecular mechanisms of the oncogenic signaling pathway(s) that are involved in prostate carcinogenesis play a crucial role in disease progression and persistence. There is an important role of signal transducer and activator of transcriptions (STATs) particularly STAT-3 and STAT-5 and its negative regulator suppressor of cytokine signaling-1 (SOCS-1).

    METHODS: In the present study, the expression and localization of STAT and SOCS-1 proteins in prostate cancer by immunohistochemistry in a total of 150 formalin-fixed, paraffin-embedded human prostate tissues of different grade obtained by radical prostatectomies or transurethral resection.

    RESULTS: A significantly strong STAT-3 expression pattern in 68% (65/95) prostate cancer cases as compared to 12% (5/55) in benign prostatic hyperplasia (BPH) controls (P < 0.001) was observed. Interestingly the SOCS-1 expression was found to be significantly elevated in prostate cancer cases (P < 0.001).

    CONCLUSIONS: The present study demonstrates overexpression of STAT-3 and STAT-5 proteins and a contrasting role of SOCS-1 in prostate cancer. These results suggest a critical association between altered expression of STAT-3 and STAT-5 with SOCS-1 and indicate its potential role as a negative regulator independent of JAK-STAT pathway in tumorigenic transformation of prostate tissue. The results of the present report focuses on the fundamental differences in major oncogenic signaling cascades between benign and malignant form of prostate tissue that plays a crucial role in prostate cancer biology.

  • 3.
    Sobti, Ranbir C.
    et al.
    Department of Biotechnology, Panjab University, Chandigarh, India.
    Singh, Neha
    Department of Biotechnology, Panjab University, Chandigarh, India.
    Hussain, Showket
    Division of Molecular Genetics and Biochemistry, Institute of Cytology & Preventive Oncology (ICMR), Noida, India.
    Suri, Vanita
    Department of Gynaecology and Obstetrics, PGIMER, Chandigarh, India.
    Bharadwaj, Mausumi
    Division of Molecular Genetics and Biochemistry, Institute of Cytology & Preventive Oncology (ICMR), Noida, India.
    Das, Bhudev C.
    Dr. B.R. Ambedkar Research Centre for Biomedical Research (ACBR), University of Delhi, India.
    Deregulation of STAT-5 isoforms in the development of HPV-mediated cervical carcinogenesis2010In: Journal of Receptor and Signal Transduction Research, ISSN 1079-9893, E-ISSN 1532-4281, Vol. 30, no 3, p. 178-188Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Cervical cancer is the second most common cancer and is leading cause of cancer related deaths in women worldwide. High Risk-Human papillomavirus (HPV) types play an important role in cervical carcinogenesis. Considering the important role of signal transducer and activator of transcription-5 (STAT-5), an important member of JAK/STAT family which plays a crucial role in various cancers and HPV as a key mediator in the development of cervical carcinogenesis, the purpose of the current study was to examine the possible relationship between HPV infection and expression of STAT-5 gene isoforms in cervical cancer.

    METHODS: A total of 120 fresh cervical tissue specimens comprising precancer (n = 12), cancer (n = 78) and normal controls (n = 30) were analyzed for HPV infection and expression pattern of STAT-5 mRNA (both isoforms STAT-5a and STAT-5b) and protein in different stages of cervical carcinoma biopsies by reverse-transcriptase-PCR, western blotting and immunohistochemistry.

    RESULTS: A significantly increased expression of STAT-5 was detected in most of the cervical tumors (P < 0.001), whereas it was almost undetectable in normal controls. Also the study of relative contribution of STAT-5 isoforms revealed a higher expression pattern of STAT-5b and was associated with severity of the disease. On the contrary, STAT-5a was found to be significantly downregulated in cervical tumor tissues (P < 0.001). HPV infection was found in 90% of the cervical cancer cases and was significantly associated with STAT-5 overexpression (P = 0.001).

    CONCLUSIONS: We observed for the first time the differential expression pattern of STAT-5 isoforms in cervical cancer and that STAT-5 may play an important role in the progression of HPV-mediated cervical cancer.

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