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102. The Role of Sarcosine Metabolism in Prostate Cancer Progression12

Author

Khan, Amjad P, Rajendiran, Thekkelnaycke M, Ateeq, Bushra, Asangani, Irfan A, Athanikar, Jyoti N, Yocum, Anastasia K, Mehra, Rohit, Siddiqui, Javed, Palapattu, Ganesh, Wei, John T, Michailidis, George, Sreekumar, Arun, and Chinnaiyan, Arul M

Subjects
Male, Mice, Inbred BALB C, Sarcosine Dehydrogenase, Gene Expression, Mice, Nude, Prostatic Neoplasms, Sarcosine, Glycine N-Methyltransferase, Middle Aged, Sarcosine Oxidase, urologic and male genital diseases, Tumor Burden, Gene Expression Regulation, Neoplastic, Mice, Case-Control Studies, Cell Line, Tumor, Biomarkers, Tumor, Disease Progression, Animals, Humans, Neoplasm Invasiveness, Neoplasm Transplantation, Research Article, Aged
Abstract

Metabolomic profiling of prostate cancer (PCa) progression identified markedly elevated levels of sarcosine (N-methyl glycine) in metastatic PCa and modest but significant elevation of the metabolite in PCa urine. Here, we examine the role of key enzymes associated with sarcosine metabolism in PCa progression. Consistent with our earlier report, sarcosine levels were significantly elevated in PCa urine sediments compared to controls, with a modest area under the receiver operating characteristic curve of 0.71. In addition, the expression of sarcosine biosynthetic enzyme, glycine N-methyltransferase (GNMT), was elevated in PCa tissues, while sarcosine dehydrogenase (SARDH) and pipecolic acid oxidase (PIPOX), which metabolize sarcosine, were reduced in prostate tumors. Consistent with this, GNMT promoted the oncogenic potential of prostate cells by facilitating sarcosine production, while SARDH and PIPOX reduced the oncogenic potential of prostate cells by metabolizing sarcosine. Accordingly, addition of sarcosine, but not glycine or alanine, induced invasion and intravasation in an in vivo PCa model. In contrast, GNMT knockdown or SARDH overexpression in PCa xenografts inhibited tumor growth. Taken together, these studies substantiate the role of sarcosine in PCa progression.

Published
2013

103. Association of AGTR1(A1166C) and ACE(I/D) Polymorphisms with Breast Cancer Risk in North Indian Population

Author

Singh, Anukriti, Srivastava, Nidhi, Amit, Sonal, Prasad, S.N., Misra, M.P., and Ateeq, Bushra

Abstract

Renin angiotensin system (RAS) comprising Angiotensin converting enzyme (ACE), Angiotensin II (Ang II) and its receptor Angiotensin II receptor type I (AGTR1), plays a critical role in several diseases including cancer. A single nucleotide polymorphism (SNP) A1166C located in 3′ untranslated region (UTR) of AGTR1and an insertion/deletion (I/D) polymorphism present in intron 16 of ACEgene have been associated with many diseases, but their association with Breast cancer (BCa) is still debatable. Here, we for the first time investigated the association of these polymorphisms in a North Indian BCa cohort including 161 patients and 152 healthy women. The polymorphisms were evaluated by polymerase chain reaction (PCR) and restriction fragment length polymorphism (RFLP) respectively. The association between these polymorphisms and BCa risk was estimated by calculating Odds Ratio (OR) and chi-square (χ2) test. The DD genotype/D allele of ACE(I/D) polymorphism and “AC and CC” genotype/C allele of AGTR1(A1166C) polymorphism were associated with higher risk of BCa when evaluated independently. Furthermore, interaction analysis of “AC and CC” and DD genotype and combination of “C and D” alleles of both polymorphisms revealed significantly greater BCa risk than that observed independently. Conclusively, women harboring “AC or CC” genotype/C allele for AGTR1(A1166C) polymorphism and DD genotype/D allele for ACE(I/D) polymorphisms have a predisposition to develop more aggressive disease with advanced staging and larger tumor size. Our study indicates importance of genetic screening based on these polymorphisms for women, who may have higher risk of BCa.

Published
2018
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104. Characterization of SPINK1 in Prostate Cancer

Author

MICHIGAN UNIV ANN ARBOR, Chinnaiyan, Arul M., Ateeq, Bushra, MICHIGAN UNIV ANN ARBOR, Chinnaiyan, Arul M., and Ateeq, Bushra

Abstract

We have used the outlier meta-analysis approach (meta-COPA) to identify SPINK1 outlier expression exclusively in a subset of ETS rearrangement-negative prostate cancers (10% of total prostate cancer cases). We have demonstrated SPINK1 expression is mutually exclusive to ETS fusion status, and SPINK1 has outlier expression in those cases. We investigated the functional role for SPINK1 in ETSfusion negative prostate cancer by generating lentiviruses expressing SPINK1 and infected the benign immortalized prostate epithelial cell line RWPE to generate stable RWPE-SPINK1 cells. Over-expression of SPINK1 had no significant effect on the proliferation of these cells. We also generated stable knockdown of SPINK1 in endogenous SPINK1 expressing 22RV1 cells. Here we have shown that SPINK1 plays important role in 22Rv1 cell proliferation, as knockdown of SPINK1 in 22RV1 cells showed a decrease in cell proliferation and colony formation. Moreover, SPINK1 knockdown also showed a decrease in cell invasion in Boyden chamber Matrigel assay and cell motility in bead motility assay., The original document contains color images.

Published
2009

105. Identification of Targetable FGFR Gene Fusions in Diverse Cancers

Author

Wu, Yi-Mi, primary, Su, Fengyun, additional, Kalyana-Sundaram, Shanker, additional, Khazanov, Nickolay, additional, Ateeq, Bushra, additional, Cao, Xuhong, additional, Lonigro, Robert J., additional, Vats, Pankaj, additional, Wang, Rui, additional, Lin, Su-Fang, additional, Cheng, Ann-Joy, additional, Kunju, Lakshmi P., additional, Siddiqui, Javed, additional, Tomlins, Scott A., additional, Wyngaard, Peter, additional, Sadis, Seth, additional, Roychowdhury, Sameek, additional, Hussain, Maha H., additional, Feng, Felix Y., additional, Zalupski, Mark M., additional, Talpaz, Moshe, additional, Pienta, Kenneth J., additional, Rhodes, Daniel R., additional, Robinson, Dan R., additional, and Chinnaiyan, Arul M., additional

Published
2013
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106. Abstract 5348: Characterization of the EZH2-MMSET histone methyltransferase regulatory axis in cancer.

Author

Asangani, Irfan A., primary, Ateeq, Bushra, additional, Cao, Qi, additional, Dodson, Lois, additional, Pandhi, Mithil, additional, Kunju, Lakshmi P., additional, Mehra, Rohit, additional, Lonigro, Robert J., additional, Siddiqui, Javed, additional, Palanisamy, Nallasivam, additional, Wu, Yi-Mi, additional, Cao, Xuhong, additional, Kim, Jung H., additional, Iyer, Mathew K., additional, Maher, Christopher A., additional, Kumar-Sinha, Chandan, additional, Varambally, Sooryanarayana, additional, Chinnaiyan, Arul M., additional, Zhao, Meng, additional, and Qin, Zhaohui S., additional

Published
2013
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107. Mechanistic Rationale for Inhibition of Poly(ADP-Ribose) Polymerase in ETS Gene Fusion-Positive Prostate Cancer

Author

Brenner, J. Chad, primary, Ateeq, Bushra, additional, Li, Yong, additional, Yocum, Anastasia K., additional, Cao, Qi, additional, Asangani, Irfan A., additional, Patel, Sonam, additional, Wang, Xiaoju, additional, Liang, Hallie, additional, Yu, Jindan, additional, Palanisamy, Nallasivam, additional, Siddiqui, Javed, additional, Yan, Wei, additional, Cao, Xuhong, additional, Mehra, Rohit, additional, Sabolch, Aaron, additional, Basrur, Venkatesha, additional, Lonigro, Robert J., additional, Yang, Jun, additional, Tomlins, Scott A., additional, Maher, Christopher A., additional, Elenitoba-Johnson, Kojo S.J., additional, Hussain, Maha, additional, Navone, Nora M., additional, Pienta, Kenneth J., additional, Varambally, Sooryanarayana, additional, Feng, Felix Y., additional, and Chinnaiyan, Arul M., additional

Published
2013
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108. Characterization of the EZH2-MMSET Histone Methyltransferase Regulatory Axis in Cancer

Author

Asangani, Irfan A., primary, Ateeq, Bushra, additional, Cao, Qi, additional, Dodson, Lois, additional, Pandhi, Mithil, additional, Kunju, Lakshmi P., additional, Mehra, Rohit, additional, Lonigro, Robert J., additional, Siddiqui, Javed, additional, Palanisamy, Nallasivam, additional, Wu, Yi-Mi, additional, Cao, Xuhong, additional, Kim, Jung H., additional, Zhao, Meng, additional, Qin, Zhaohui S., additional, Iyer, Mathew K., additional, Maher, Christopher A., additional, Kumar-Sinha, Chandan, additional, Varambally, Sooryanarayana, additional, and Chinnaiyan, Arul M., additional

Published
2013
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109. Role of Transcriptional Corepressor CtBP1 in Prostate Cancer Progression

Author

Wang, Rui, primary, Asangani, Irfan A, additional, Chakravarthi, Balabhadrapatruni VSK, additional, Ateeq, Bushra, additional, Lonigro, Robert J, additional, Cao, Qi, additional, Ram-Shankar, Mani, additional, Camacho, Daniel F, additional, McGregor, Natalie, additional, Schumann, Taibriana EW, additional, Jing, Xiaojun, additional, Menawat, Radhika, additional, Tomlins, Scott A, additional, Zheng, Heng, additional, Otte, Arie P, additional, Mehra, Rohit, additional, Siddiqui, Javed, additional, Dhanasekaran, Saravana M, additional, Nyati, Mukesh K, additional, Pienta, Kenneth J, additional, Palanisamy, Nallasivam, additional, Kunju, Lakshmi P, additional, Rubin, Mark A, additional, Chinnaiyan, Arul M, additional, and Varambally, Sooryanarayana, additional

Published
2012
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110. Characterization of KRAS Rearrangements in Metastatic Prostate Cancer

Author

Wang, Xiao-Song, primary, Shankar, Sunita, additional, Dhanasekaran, Saravana M., additional, Ateeq, Bushra, additional, Sasaki, Atsuo T., additional, Jing, Xiaojun, additional, Robinson, Daniel, additional, Cao, Qi, additional, Prensner, John R., additional, Yocum, Anastasia K., additional, Wang, Rui, additional, Fries, Daniel F., additional, Han, Bo, additional, Asangani, Irfan A., additional, Cao, Xuhong, additional, Li, Yong, additional, Omenn, Gilbert S., additional, Pflueger, Dorothee, additional, Gopalan, Anuradha, additional, Reuter, Victor E., additional, Kahoud, Emily Rose, additional, Cantley, Lewis C., additional, Rubin, Mark A., additional, Palanisamy, Nallasivam, additional, Varambally, Sooryanarayana, additional, and Chinnaiyan, Arul M., additional

Published
2011
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112. Abstract 2795: An onco-protein axis linking polycomb repressive complex 2 and polycomb repressive complex 1 through miRNAs in cancer

Author

Cao, Qi, primary, Mani, Ram, additional, Ateeq, Bushra, additional, Dhanasekaren, Saravana M., additional, Asangani, Irfan, additional, Yu, Jindan, additional, Prensner, John, additional, Kim, Jung J., additional, Brenner, J. Chad, additional, Cao, Xuhong, additional, Jing, Xiaojun, additional, Wang, Rui, additional, Li, Yong, additional, Dahiya, Arun, additional, Wang, Lei, additional, Lonigro, Robert, additional, Tomlins, Scott, additional, Palanisamy, Nallasivam, additional, Maher, Christopher, additional, Varambally, Sooryanarayana, additional, and Chinnaiyan, Arul M., additional

Published
2011
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113. Abstract 2808: Characterization of KRAS rearrangements in metastatic prostate cancer

Author

Wang, Xiao-Song, primary, Shankar, Sunita, additional, Dhanasekaran, Saravana M., additional, Ateeq, Bushra, additional, Sasaki, Atsuo T., additional, Jing, Xiaojun, additional, Robinson, Daniel, additional, Cao, Qi, additional, Gopalan, Anuradha, additional, Reuter, Victor E., additional, Cantley, Lewis C., additional, Rubin, Mark A., additional, Palanisamy, Nallasivam, additional, Varambally, Sooryanarayana, additional, and Chinnaiyan, Arul M., additional

Published
2011
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114. Abstract 953: Mechanistic rationale for inhibition of Poly(ADP-Ribose) Polymerase in ETS gene fusion positive prostate cancer

Author

Brenner, J. Chad, primary, Ateeq, Bushra, additional, Li, Yong, additional, Yocum, Anastasia, additional, Cao, Qi, additional, Asangani, Irfan, additional, Patel, Sonam, additional, Liang, Hallie, additional, Yu, Jindan, additional, Palanisamy, Nallasivam, additional, Siddiqui, Javed, additional, Yan, Wei, additional, Wang, Xiaoju, additional, Cao, Xuhong, additional, Mehra, Rohit, additional, Basrur, Venkatesha, additional, Lonigro, Robert, additional, Yang, Jun, additional, Tomlins, Scott, additional, Maher, Christopher, additional, Elenitoba-Johnson, Kojo, additional, Hussain, Maha, additional, Navone, Nora M., additional, Pienta, Kenneth, additional, Varambally, Sooryanarayana, additional, Feng, Felix Y., additional, and Chinnaiyan, Arul M., additional

Published
2011
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115. Therapeutic Targeting of SPINK1-Positive Prostate Cancer

Author

Ateeq, Bushra, primary, Tomlins, Scott A., additional, Laxman, Bharathi, additional, Asangani, Irfan A., additional, Cao, Qi, additional, Cao, Xuhong, additional, Li, Yong, additional, Wang, Xiaoju, additional, Feng, Felix Y., additional, Pienta, Kenneth J., additional, Varambally, Sooryanarayana, additional, and Chinnaiyan, Arul M., additional

Published
2011
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117. Rearrangements of the RAF kinase pathway in prostate cancer, gastric cancer and melanoma

Author

Palanisamy, Nallasivam, primary, Ateeq, Bushra, additional, Kalyana-Sundaram, Shanker, additional, Pflueger, Dorothee, additional, Ramnarayanan, Kalpana, additional, Shankar, Sunita, additional, Han, Bo, additional, Cao, Qi, additional, Cao, Xuhong, additional, Suleman, Khalid, additional, Kumar-Sinha, Chandan, additional, Dhanasekaran, Saravana M, additional, Chen, Ying-bei, additional, Esgueva, Raquel, additional, Banerjee, Samprit, additional, LaFargue, Christopher J, additional, Siddiqui, Javed, additional, Demichelis, Francesca, additional, Moeller, Peter, additional, Bismar, Tarek A, additional, Kuefer, Rainer, additional, Fullen, Douglas R, additional, Johnson, Timothy M, additional, Greenson, Joel K, additional, Giordano, Thomas J, additional, Tan, Patrick, additional, Tomlins, Scott A, additional, Varambally, Sooryanarayana, additional, Rubin, Mark A, additional, Maher, Christopher A, additional, and Chinnaiyan, Arul M, additional

Published
2010
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121. Abstract B90: Genomic loss of a microRNA leads to overexpression of EZH2 in cancer

Author

Cao, Qi, primary, Varambally, Sooryanarayana, additional, Mani, Ram-Shankar, additional, Shankar, Sunita, additional, Wang, Xiaosong, additional, Ateeq, Bushra, additional, Laxman, Bharathi, additional, Brenner, J. Chad, additional, Kim, Jung, additional, Cao, Xuhong, additional, Han, Bo, additional, Kumar-Sinha, Chandan, additional, Tan, Patrick, additional, Palanisamy, Nallasivam, additional, Lonigro, Robert, additional, Maher, Christopher, additional, and Chinnaiyan, Arul, additional

Published
2008
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127. The Role of Sarcosine Metabolism in Prostate Cancer Progression.

Author

Khan, Amjad P., Rajendiran, Thekkelnaycke M., Ateeq, Bushra, Asangani, Irfan A., Athanikar, Jyoti N., Yocum, Anastasia K., Mehra, Rohit, Siddiqui, Javed, Palapattu, Ganesh, Wei, John T., Michailidis, George, Sreekumar, Arun, and Chinnaiyan, Arul M.

Subjects
*PROSTATE cancer, *CANCER invasiveness, *GLYCINE, *METHYLTRANSFERASES, *CANCER cells
Abstract

Metabolomic profiling of prostate cancer (PCa) progression identified markedly elevated levels of sarcosine (N-methyl glycine) in metastatic PCa and modest but significant elevation of the metabolite in PCa urine. Here, we examine the role of key enzymes associated with sarcosine metabolism in PCa progression. Consistent with our earlier report, sarcosine levels were significantly elevated in PCa urine sediments compared to controls, with a modest area under the receiver operating characteristic curve of 0.71. In addition, the expression of sarcosine biosynthetic enzyme, glycine N-methyltransferase (GNMT), was elevated in PCa tissues, while sarcosine dehydrogenase (SARDH) and pipecolic acid oxidase (PIPOX), which metabolize sarcosine, were reduced in prostate tumors. Consistent with this, GNMT promoted the oncogenic potential of prostate cells by facilitating sarcosine production, while SARDH and PIPOX reduced the oncogenic potential of prostate cells by metabolizing sarcosine. Accordingly, addition of sarcosine, but not glycine or alanine, induced invasion and intravasation in an in vivo PCa model. In contrast, GNMT knockdown or SARDH overexpression in PCa xenografts inhibited tumor growth. Taken together, these studies substantiate the role of sarcosine in PCa progression. [ABSTRACT FROM AUTHOR]

Published
2013
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128. Role of Transcriptional Corepressor CtBP1 in Prostate Cancer Progression.

Author

Rui Wang, Asangani, Irfan A., Chakravarthi, Balabhadrapatruni V. S. K., Ateeq, Bushra, Lonigro, Robert J., Qi Cao, Mani, Ram-Shankar, Camacho, Daniel F., McGregor, Natalie, Schumann, Taibriana E. W., Xiaojun Jing, Menawat, Radhika, Tomlins, Scott A., Heng Zheng, Otte, Arie P., Mehra, Rohit, Siddiqui, Javed, Dhanasekaran, Saravana M., Nyati, Mukesh K., and Pienta, Kenneth J.

Subjects
*PROSTATE cancer, *CANCER invasiveness, *C-terminal binding proteins, *CANCER cells, *CELL lines
Abstract

Transcriptional repressors and corepressors play a critical role in cellular homeostasis and are frequently altered in cancer. C-terminal binding protein 1 (CtBP1), a transcriptional corepressor that regulates the expression of tumor suppressors and genes involved in cell death, is known to play a role in multiple cancers. In this study, we observed the overexpression and mislocalization of CtBP1 in metastatic prostate cancer and demonstrated the functional significance of CtBP1 in prostate cancer progression. Transient and stable knockdown of CtBP1 in prostate cancer cells inhibited their proliferation and invasion. Expression profiling studies of prostate cancer cell lines revealed that multiple tumor suppressor genes are repressed by CtBP1. Furthermore, our studies indicate a role for CtBP1 in conferring radiation resistance to prostate cancer cell lines. In vivo studies using chicken chorioallantoic membrane assay, xenograft studies, and murine metastasis models suggested a role for CtBP1 in prostate tumor growth and metastasis. Taken together, our studies demonstrated that dysregulated expression of CtBP1 plays an important role in prostate cancer progression and may serve as a viable therapeutic target. [ABSTRACT FROM AUTHOR]

Published
2012
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129. Computational Design of BH3-Mimetic Peptide Inhibitors That Can Bind Specifically to Mcl-1 or Bcl-X L : Role of Non-Hot Spot Residues.

Author

Reddy CN, Manzar N, Ateeq B, and Sankararamakrishnan R

Subjects
Amino Acid Sequence, Humans, MCF-7 Cells, Models, Molecular, Myeloid Cell Leukemia Sequence 1 Protein chemistry, Protein Binding, Protein Domains, Substrate Specificity, bcl-X Protein chemistry, Myeloid Cell Leukemia Sequence 1 Protein antagonists & inhibitors, Myeloid Cell Leukemia Sequence 1 Protein metabolism, Peptidomimetics chemistry, Peptidomimetics pharmacology, bcl-X Protein antagonists & inhibitors, bcl-X Protein metabolism
Abstract

Interactions between pro- and anti-apoptotic Bcl-2 proteins decide the fate of the cell. The BH3 domain of pro-apoptotic Bcl-2 proteins interacts with the exposed hydrophobic groove of their anti-apoptotic counterparts. Through their design and development, BH3 mimetics that target the hydrophobic groove of specific anti-apoptotic Bcl-2 proteins have the potential to become anticancer drugs. We have developed a novel computational method for designing sequences with BH3 domain features that can bind specifically to anti-apoptotic Mcl-1 or Bcl-X L . In this method, we retained the four highly conserved hydrophobic and aspartic residues of wild-type BH3 sequences and randomly substituted all other positions to generate a large number of BH3-like sequences. We modeled 20000 complex structures with Mcl-1 or Bcl-X L using the BH3-like sequences derived from five wild-type pro-apoptotic BH3 peptides. Peptide-protein interaction energies calculated from these models for each set of BH3-like sequences resulted in negatively skewed extreme value distributions. The selected BH3-like sequences from the extreme negative tail regions have highly favorable interaction energies with Mcl-1 or Bcl-X L . They are enriched in acidic and basic residues when they bind to Mcl-1 and Bcl-X L , respectively. With the charged residues often away from the binding interface, the overall electric field generated by the charged residues results in strong long-range electrostatic interaction energies between the peptide and the protein giving rise to high specificity. Cell viability studies of representative BH3-like peptides further validated the predicted specificity. This study has revealed the importance of non-hot spot residues in BH3-mimetic peptides in providing specificity to a particular anti-apoptotic protein.

Published
2020
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