Rugang Zhang
Wistar Institute
CancerMolecular biologyOvarian cancerCancer researchBiology
What is this?
Publications 100
#1Bo Zhao (Wistar Institute)H-Index: 1
#2Pingyu Liu (Wistar Institute)H-Index: 1
Last. Qin Liu (Wistar Institute)H-Index: 28
view all 12 authors...
Cyclic cGMP-AMP synthase (cGAS) is a pattern recognition cytosolic DNA sensor that is essential for cellular senescence. cGAS promotes inflammatory senescence-associated secretory phenotype (SASP) through recognizing cytoplasmic chromatin during senescence. cGAS-mediated inflammation is essential for the antitumor effects of immune checkpoint blockade. However, the mechanism by which cGAS recognizes cytoplasmic chromatin is unknown. Here we show that topoisomerase 1-DNA covalent cleavage complex...
#1Jiao Yuan (UPenn: University of Pennsylvania)H-Index: 4
#2Kevin H. Kensler (Harvard University)H-Index: 2
Last. Kathleen T. Montone (UPenn: University of Pennsylvania)H-Index: 39
view all 16 authors...
Men of predominantly African Ancestry (AA) have higher prostate cancer (CaP) incidence and worse survival than men of predominantly European Ancestry (EA). While socioeconomic factors drive this disparity, genomic factors may also contribute to differences in the incidence and mortality rates. To compare the prevalence of prostate tumor genomic alterations and transcriptomic profiles by patient genetic ancestry, we evaluated genomic profiles from The Cancer Genome Atlas (TCGA) CaP cohort (n = 49...
1 CitationsSource
#1Jing Li (UM: University of Michigan)H-Index: 1
#1Jing LiH-Index: 49
Last. Wei LiH-Index: 28
view all 25 authors...
Whether mutations in cancer driver genes directly affect cancer immune phenotype and T cell immunity remains a standing question. ARID1A is a core member of the polymorphic BAF chromatin remodeling complex. ARID1A mutations occur in human cancers and drive cancer development. Here, we studied the molecular, cellular, and clinical impact of ARID1A aberrations on cancer immunity. We demonstrated that ARID1A aberrations resulted in limited chromatin accessibility to interferon (IFN) responsive gene...
#1Sergey Karakashev (Wistar Institute)H-Index: 3
#2Takeshi Fukumoto (Wistar Institute)H-Index: 10
Last. Mark G. CadungogH-Index: 5
view all 14 authors...
Summary In response to DNA double-strand breaks, MAD2L2-containing shieldin complex plays a critical role in the choice between homologous recombination (HR) and non-homologous end-joining (NHEJ)-mediated repair. Here we show that EZH2 inhibition upregulates MAD2L2 and sensitizes HR-proficient epithelial ovarian cancer (EOC) to poly(adenosine diphosphate-ribose) polymerase (PARP) inhibitor in a CARM1-dependent manner. CARM1 promotes MAD2L2 silencing by driving the switch from the SWI/SNF complex...
1 CitationsSource
#1Takeshi Fukumoto (Wistar Institute)H-Index: 10
#2Nail Fatkhutdinov (Kazan: Kazan Federal University)H-Index: 6
Last. Rugang Zhang (Wistar Institute)H-Index: 32
view all 10 authors...
ARID1A, encoding a subunit of the SWI/SNF complex, is the most frequently mutated epigenetic regulator in human cancers and is mutated in over 50% of ovarian clear cell carcinoma (OCCC), a disease that currently has no effective therapy. Inhibition of histone deacetylase 6 (HDAC6) suppresses the growth of ARID1A-mutated tumors and modulates the tumor immune microenvironment. Here we show that inhibition of HDAC6 synergizes with anti-PD-L1 immune-checkpoint blockade in ARID1A-inactivated ovarian ...
2 CitationsSource
#1Bo Zhao (Wistar Institute)H-Index: 1
#2Jianhuang Lin (Wistar Institute)H-Index: 3
Last. Rugang Zhang (Wistar Institute)H-Index: 32
view all 17 authors...
ARID1A inactivation causes mitotic defects. Paradoxically, cancers with high ARID1A mutation rates typically lack copy number alterations (CNAs). Here, we show that ARID1A inactivation causes defects in telomere cohesion, which selectively eliminates gross chromosome aberrations during mitosis. ARID1A promotes the expression of cohesin subunit STAG1 that is specifically required for telomere cohesion. ARID1A inactivation causes telomere damage that can be rescued by STAG1 expression. Colony form...
3 CitationsSource
#1Timothy Nacarelli (Wistar Institute)H-Index: 4
#2Rugang Zhang (Wistar Institute)H-Index: 32
ABSTRACTWe have recently discovered that nicotinamide adenine dinucleotide metabolism controls the pro-inflammatory senescence-associated secretory phenotype during cellular senescence. This newly ...
#1Robert C. Bast (University of Texas MD Anderson Cancer Center)H-Index: 104
#2Ursula A. Matulonis (Harvard University)H-Index: 56
Last. Lee Zou (Harvard University)H-Index: 39
view all 43 authors...
5 CitationsSource
#1Shuai Wu (Wistar Institute)H-Index: 5
#2Nail Fatkhutdinov (Kazan: Kazan Federal University)H-Index: 6
Last. Rugang Zhang (Wistar Institute)H-Index: 32
view all 13 authors...
ARID1A, a subunit of the SWItch/Sucrose Non-Fermentable (SWI/SNF) chromatin-remodeling complex, localizes to both promoters and enhancers to influence transcription. However, the role of ARID1A in higher-order spatial chromosome partitioning and genome organization is unknown. Here, we show that ARID1A spatially partitions interphase chromosomes and regulates higher-order genome organization. The SWI/SNF complex interacts with condensin II, and they display significant colocalizations at enhance...
1 CitationsSource
#1Takeshi Fukumoto (Wistar Institute)H-Index: 10
#2Hengrui Zhu (Wistar Institute)H-Index: 8
Last. Rugang Zhang (Wistar Institute)H-Index: 32
view all 12 authors...
Despite the high initial response rates to PARP inhibitors (PARPi) in BRCA-mutated epithelial ovarian cancers (EOC), PARPi resistance remains a major challenge. Chemical modifications of RNAs have emerged as a new layer of epigenetic gene regulation. N6-methyladenosine (m6A) is the most abundant chemical modification of messenger RNA (mRNA), yet the role of m6A modification in PARPi resistance has not previously been explored. Here we show that m6A modification of FZD10 mRNA contributes to PARPi...