Research Profile
Dr. Anshu Singh is a cancer biologist whose research spans epigenetics, DNA damage response, and metabolic reprogramming in lung cancer. Her work contributes to understanding how chromatin-level changes and nuclear architecture alterations drive tumor progression, immune evasion, and metastasis.
Published in high-impact journals including Nature Communications and the Journal of Experimental Medicine, Dr. Singh's research has uncovered key molecular mechanisms by which epigenetic regulators — including RNF20 and Lamin B1 — function as tumor suppressors in lung cancer. Her findings have direct implications for the development of targeted therapies and immunotherapeutic strategies.
Dr. Singh's work aligns closely with the cancer immunoediting framework: understanding how epigenetic and metabolic changes within tumor cells shape their interaction with the immune system — from initial recognition to immune escape.
Research Focus Areas
Epigenetic Regulation in Cancer
Investigating how histone modifications and chromatin remodelers control oncogene activation and tumor suppressor silencing.
Lung Cancer Biology
Mechanistic studies of lung adenocarcinoma and small cell lung cancer, from early transformation to metastatic spread.
Metabolic Reprogramming
Exploring how HIF1α-driven glycolysis and metabolic rewiring promote tumor survival and immune cell exclusion.
DNA Damage & Immune Response
Linking DNA repair defects to neoantigen generation and altered immune recognition in the context of immunoediting.
Featured Research
RNF20 links the DNA damage response and metabolic rewiring in lung cancer through HIF1α
This study reveals that RNF20-mediated monoubiquitination of histone H2B controls Rbx1 expression and VHL ubiquitin ligase activity, regulating HIF1α levels. Loss of even one Rnf20 allele dramatically increases lung tumor incidence in mice, with mechanisms involving the Rnf20–H2Bub1–p53 pathway alongside HIF1α-mediated metabolic reprogramming independent of H2Bub1.
Key Findings
- Rnf20 haploinsufficiency triggers spontaneous lung adenocarcinoma and small cell lung cancer formation in mice
- RNF20-deficient tumor cells exhibit pronounced defects in DNA double-strand break repair
- Enhanced glycolysis through HIF1α activation drives glucose uptake and lactate production in RNF20-depleted tumors
- Decreased RNF20 correlates with elevated HIF1α and poor patient survival in adenocarcinoma
- HIF1α inhibition or glucose uptake blockade rescues the proliferative and metastatic phenotypes
Lamin B1 loss promotes lung cancer development and metastasis by epigenetic derepression of RET
This work identifies Lamin B1 — a structural component of the nuclear lamina — as a tumor suppressor in lung cancer. Reduced Lamin B1 levels promote epithelial-mesenchymal transition (EMT) and tumor progression by causing epigenetic derepression of the RET proto-oncogene. The mechanism involves altered histone methylation patterns that activate RET signaling, driving both cancer development and metastatic spread.
Key Findings
- Lamin B1 acts as a tumor suppressor in lung cancer; its loss accelerates malignant transformation
- Reduced Lamin B1 epigenetically derepresses the RET proto-oncogene via altered histone methylation
- RET reactivation promotes epithelial-mesenchymal transition (EMT) and metastatic behavior
- Nuclear architecture disruption directly shapes the epigenetic landscape of oncogene expression
- Findings implicate the nuclear lamina as a regulatory layer in cancer immunoediting and escape
Interested in Collaboration?
Dr. Singh welcomes inquiries from researchers and clinicians working at the intersection of epigenetics, cancer immunology, and translational oncology.