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10 results on '"Saini, Taruna"'

1. Performance Analysis of Different Machine Learning Classifiers for Prediction of Lung Cancer

Author

Saini, Taruna, Chhabra, Amit, Filipe, Joaquim, Editorial Board Member, Ghosh, Ashish, Editorial Board Member, Prates, Raquel Oliveira, Editorial Board Member, Zhou, Lizhu, Editorial Board Member, Challa, Rama Krishna, editor, Aujla, Gagangeet Singh, editor, Mathew, Lini, editor, Kumar, Amod, editor, Kalra, Mala, editor, Shimi, S. L., editor, Saini, Garima, editor, and Sharma, Kanika, editor

Published
2024
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3. Contributors

Author

Abdullaev, Bekhzod, primary, Afzal, Mohammad, additional, Ahmad, Faizan, additional, Ahmad, Javed, additional, Alam, Manzar, additional, Ali, Sabeeha, additional, Annadurai, Narendran, additional, Anwar, Saleha, additional, Ara, Shabnam Anjum, additional, Badar, Sufian, additional, Bagheri, Soghra, additional, Banerjee, Subhamoy, additional, Bhat, Eijaz Ahmed, additional, Bhatt, Hardik, additional, Bisht, Deepa, additional, Dan, Siddhartha, additional, Das, Debasis, additional, Das, Viswanath, additional, Dhankhar, Poonam, additional, Dube, Divya, additional, Gupta, Parth, additional, Gupta, Varsha, additional, Hassan, Md. Imtaiyaz, additional, Hekmat, Azadeh, additional, Hyderi, Zeeshan, additional, Islam, Asimul, additional, James, Michael N.G., additional, Jha, Hem Chandra, additional, Jit, Bimal Prasad, additional, Kashyap, Dharmendra, additional, Kaur, Lajpreet, additional, Khan, Md Khurshid Alam, additional, Khan, Mohammad Ahmed, additional, Kumar, Dhiraj, additional, Kumar, Pravindra, additional, Kumar, Vinod, additional, Kumari, Varsha, additional, Mishra, Parul, additional, Misra, Ashish, additional, Mittal, Disha, additional, Mittal, Pooja, additional, Mohammad, Taj, additional, Musvi, Syed Shahid, additional, Nagar, Garima, additional, Naqi, Asma, additional, Nayak, Chirasmita, additional, Niveria, Karishma, additional, Noor, Saba, additional, Ojha, Himanshu, additional, Padhy, Amrita Arpita, additional, Pathak, Mallika, additional, Pathak, Upasana, additional, Payoe, Roshani, additional, Rai, Sandhya, additional, Rani, Annu, additional, Rankawat, Sourbh, additional, Raut, Rajnikant, additional, Raza, Ali, additional, Rustagi, Vanshika, additional, Saboury, Ali Akbar, additional, Sachan, Manisha, additional, Sahoo, Subhashree, additional, Saini, Taruna, additional, Sajjad, Nasreena, additional, Shakeel, Ilma, additional, Shamsi, Anas, additional, Shamsi, Tooba Naz, additional, Sharma, Saroj, additional, Shaw, Suman, additional, Shivani, Kummari, additional, Singh, Archana, additional, Singh, Indrakant Kumar, additional, Singh, Sanjeev Kumar, additional, Singh, Vishakha, additional, Singhal, Rahul, additional, Srivastava, Ankit, additional, Srivastava, Sameer, additional, Tiwari, Deeksha, additional, Tiwari, Vishvanath, additional, Varshney, Nidhi, additional, Verma, Anita Kamra, additional, Vishwakarma, Keerti, additional, and Zaidi, Yeshfa, additional

Published
2022
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7. Src kinase: An attractive therapeutic target for prostate cancer

Author

Raut, Rajnikant, Gupta, Parth, Saini, Taruna, Mishra, Parul, Misra, Ashish, Raut, Rajnikant, Gupta, Parth, Saini, Taruna, Mishra, Parul, and Misra, Ashish

Abstract

Prostate cancer is an extremely complex multifactorial disease that poses a major health problem to men worldwide. Metastasis to distant sites is the underlying basis of poor prognosis and high fatality in patients with prostate cancer. Numerous protein kinase families are associated with prostate cancer tumorigenesis, and their members either individually and/or collectively drive its progression. SFKs belonging to the nonreceptor tyrosine kinase family play critical roles in signaling pathways that are frequently altered in cancers. In prostate cancer, these kinases activate pathways linked to increased invasiveness, angiogenesis, metastasis, and poor response to known therapeutics. A number of SFK inhibitors have demonstrated immense promise in preclinical cancer models and are currently in different stages of clinical trials. In this chapter, we discuss the role of these kinases in prostate cancer tumorigenesis and the clinical relevance and challenges associated with the usage of SFK inhibitors in clinics. © 2022 Elsevier Inc. All rights reserved.

Published
2022

10. Insulin-Like Growth Factor 2 mRNA-Binding Protein 2 (IGF2BP2) Promotes Castration-Resistant Prostate Cancer Progression by Regulating AR-V7 mRNA Stability.

Author

Saini T, Srivastava D, Raut R, Mishra P, and Misra A

Subjects
Humans, Male, Cell Line, Tumor, Nitriles, Benzamides, RNA, Messenger genetics, Cell Proliferation, Insulin-Like Peptides, Prostatic Neoplasms, Castration-Resistant genetics, Prostatic Neoplasms, Castration-Resistant pathology, Prostatic Neoplasms, Castration-Resistant drug therapy, Receptors, Androgen metabolism, Receptors, Androgen genetics, RNA-Binding Proteins metabolism, RNA-Binding Proteins genetics, RNA Stability, Drug Resistance, Neoplasm genetics, Gene Expression Regulation, Neoplastic, Phenylthiohydantoin pharmacology, Phenylthiohydantoin analogs & derivatives, Phenylthiohydantoin therapeutic use, Disease Progression
Abstract

Background: The emergence of constitutively active androgen receptor (AR) splice variant AR-V7 poses a formidable challenge in treating prostate cancer, as it lacks the ligand binding region targeted by androgen-deprivation therapies such as enzalutamide and abiraterone. AR-V7 is critical for castration-resistant prostate cancer (CRPC) development and progression; however, the molecular mechanisms regulating its expression and biological function remain poorly understood. Here, we investigate the role of IGF2BP2 in regulating AR-V7 expression and CRPC progression., Methods: To determine the clinical relevance of IGF2BP2 in CRPC, we analyzed the mRNA expression data for prostate cancer patients available in the Genomic Data Commons (GDC) Data Portal and cBioPortal. Next to investigate the role of IGF2BP2 in regulating AR-V7 expression and enzalutamide resistance, we performed shRNA-mediated IGF2BP2 knockdown and overexpression experiments followed by qRT-PCR, immunoblot, colony-formation, and MTT assays. Finally, we performed RIP-qPCR, actinomycin-D, and IGF2BP2 domain-deletion analysis to study the mechanism by which IGF2BP2 regulates AR-V7 stability, expression, and enzalutamide resistance in CRPC cells., Results: Our analysis revealed that IGF2BP2 is upregulated in CRPC patients and its expression positively correlates with increasing Gleason score in patients with CRPC. We demonstrate that IGF2BP2 silencing leads to downregulation of AR-V7 and its downstream target genes without affecting AR levels. Additionally, IGF2BP2 knockdown also enhances the sensitivity of CRPC cells to enzalutamide while overexpression increases AR-V7 expression and confers increased resistance to enzalutamide. Mechanistically, our experiments demonstrate that IGF2BP2 binds to the intronic splicing enhancer (ISE) region of AR-V7, thereby enhancing its mRNA stability. Furthermore, our domain-deletion analysis pinpoints the role of KH3 and KH4 domains of IGF2BP2 in regulating AR-V7 stability and enzalutamide resistance., Conclusions: Taken together, our findings suggest that IGF2BP2 plays a critical role in regulating AR-V7 expression and stability, offering a novel target for developing therapeutic interventions for CRPC., (© 2025 The Author(s). Cancer Reports published by Wiley Periodicals LLC.)

Published
2025
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