J
Jing Fang
Researcher at University of Illinois at Chicago
Publications - 6
Citations - 1438
Jing Fang is an academic researcher from University of Illinois at Chicago. The author has contributed to research in topics: Carcinogenesis & Cell growth. The author has an hindex of 5, co-authored 6 publications receiving 1380 citations.
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Journal ArticleDOI
Effects of p21Waf1/Cip1/Sdi1 on cellular gene expression: implications for carcinogenesis, senescence, and age-related diseases.
Bey-Dih Chang,Keiko Watanabe,Eugenia V. Broude,Jing Fang,Jason C. Poole,Tatiana V. Kalinichenko,Igor B. Roninson +6 more
TL;DR: The results suggest that the effects of p21 induction on gene expression in senescent cells may contribute to the pathogenesis of cancer and age-related diseases.
Journal ArticleDOI
Role of p53 and p21waf1/cip1 in senescence-like terminal proliferation arrest induced in human tumor cells by chemotherapeutic drugs.
Bey-Dih Chang,Yongzhi Xuan,Eugenia V. Broude,Hongming Zhu,Brigitte Schott,Jing Fang,Igor B. Roninson +6 more
TL;DR: The results indicate that p53 and p21 act as positive regulators of senescence-like terminal proliferation arrest, but their function is neither sufficient nor absolutely required for this treatment response in tumor cells.
Journal ArticleDOI
Molecular determinants of terminal growth arrest induced in tumor cells by a chemotherapeutic agent
TL;DR: Elucidation of molecular changes in tumor cells that undergo drug-induced senescence suggests potential strategies for diagnostics and therapeutic modulation of this antiproliferative response in cancer treatment.
Journal ArticleDOI
p21Waf1/Cip1/Sdi1-induced growth arrest is associated with depletion of mitosis-control proteins and leads to abnormal mitosis and endoreduplication in recovering cells.
Bey-Dih Chang,Eugenia V. Broude,Jing Fang,Tatiana V. Kalinichenko,Ravil Abdryashitov,Jason C. Poole,Igor B. Roninson +6 more
TL;DR: In this article, p21 overexpression from an inducible promoter resulted in senescence-like growth arrest in a human fibrosarcoma cell line and after release from p21-induced growth arrest, cells re-entered the cell cycle but displayed growth retardation, cell death and decreased clonogenicity.
Journal ArticleDOI
Retinoid-induced growth arrest of breast carcinoma cells involves co-activation of multiple growth-inhibitory genes.
TL;DR: CDNA microarray hybridization and reverse transcription-polymerase chain reaction analysis showed that retinoid-induced growth arrest in MCF-7 cells is associated with strong induction of 13 genes that have antiproliferative activity, suggesting that these genes are indirectly induced by retinoids.