Jingqi Pei

Inhibition of mitotic spindle formation for TP53 mutation (TP53-mut) AML treatment using the novel compound.

• RNAseq analysis of AML samples with and without TP53 mutation.
• Inhibition of certain gene of interest using novel compounds.
• Determine cell viability, biomarkers expression, and cell cycle progression using high-throughput flow cytometry assay.
• In vivo validation of the observation using xenograft model.

Investigation of fatty acid metabolism changes in AML and investigating novel antibodies' anti-leukemic efficacy in AML.

• Inhibition of certain gene of interest using novel antibodies.
• Determine cell viability and biomarkers expression using flow cytometry assay, or lightsheet microscopy imaging.

Development of novel, combinatorial anti-leukemic treatment via high-throughput screening and proximity assays.

• Combinatorial inhibition of AML growth using appropriate agents.
• Determine cell viability, biomarkers expression, and cell cycle progression using high-throughput flow cytometry assay.
• In vivo validation of the observation using xenograft model.

• Study of metabolism changes in acute myeloid leukemia.
• Crispr-Cas editing of AML cell lines to KO specific genes.
• Development of AML therapy by utilizing AML specific super enhancers.
• In vitro confocal imaging of AML gene locus.

Development of a high-throughput screening assay for identification of mitocans

• Comparison of target cells' viability under mitocan treatments via multiple cytotoxicity assays.
• Optimization of Hoechst/PI dual-stainning method for lab automated fluorescent imaging.

Utilizing synergetic potential of mitochondria-targeting drugs for leukemia treatment development.

• Measurement of target cells' viability under mitocan or mitocan combinations treatments via Hoechst/PI dual-stainning cytotoxicity assays.
• Calculation of synergy score via Bliss model in Rstudio.
• Optimization of synergy score calculation and visualization algorithm.
• Measurement of mitochondria bioenergetic parameters via multiple commercialized biochemical assays.
• Isolation of human PBMC from source leukocytes of health or leukemia patients.

Identification of mitophagy activators PINK-1 stabilizing (PS) compounds in C. elegans model

• Identification of PS molecules in C.elegans reporter strains.
• Paralysis assay for the screening of PS molecules in C.elegans strain of Alzheimer's disease model.
• Measurement of target cells' viability under PS combinations treatments via Hoechst/PI dual-stainning cytotoxicity assays.

Study of mechanisms of novel PINK-1 stabilizers' selectivity in human leukemic cells

• Measurement of target cells' viability under PS compounds or PS combinations treatments via Hoechst/PI dual-stainning cytotoxicity assays.
• Calculation of synergy score via Bliss model in Rstudio.
• Measurement of mitochondria bioenergetic parameters via multiple commercialized biochemical assays.
• Isolation of human PBMC from source leukocytes of health or leukemia patients.

Key achievements:

1. Discovered and optimized a high-throughput screening cytotoxicity assay for mitocan selection.

2. Discovered the changes in mitochondrial bioenergetic parameters in leukemia.

3. Observed sensitivity of leukemia (both in cell lines and in primary cells) to mitochondria-targeting drugs and their combinations with typical chemotherapeutic agents.

4. Identified 8 PS molecules that indcue mitophagy activation in C.elegans.

5. Discovered potential neuroprotective effect of PS molecules in C.elegans model of Alzheimer's disease.

6. Verified cytotoxicity of PS compounds in human glial and epithelial cells.

7. Discovered the changes in mitochondrial bioenergetic parameters in leukemia.

8. Discovered sensitivity of leukemia (both in cell lines and in primary cells) to PS compounds and their combinations with typical chemotherapeutic agents.

9. Observed the potential of PS compounds that induced caspase-independent cell death mechanism (ferroptosis and necroptosis) in leukemia upon caspase inhibition.

Study of a non-human sialic acid's immunosuppression effect to innate immune system via Siglec pathway.

• Culture and maintenance of human cancer cell lines
• Viral transduction of sialidase encoding genes in HEK-293 cells
• Isolation of PBMC from source leukocytes
• Purification of NK cells from PBMC.
• Measurement of target cells' viability via multiple cytotoxicity assays
• Multi-color flow-cytometry analysis of sialic acids expression on target cells

Expanding genetic code with a non-canonical amino acids.

• Plasmid construction of pAcBac1-chPylRS, pAcBac1-Pyl-EGFP* for screening of non-canonical amino acids incorportation rate.
• Non-canonical amino acid incorporation in mammalian cell lines

Key achievements:

1. Built lab standard for cancer lines and human primary cell culture.

2. Drafted protocols for viral transduction, flow-cytometry, cytotoxicity assay protocol and PBMC isolation.

3. Observed NK killing resistance in multiple breast cancer cell lines with over-expression of Neu5Gc sialic acid. The resistance of NK induced killing effect on cancer cells is removed when Neu5Gc was removed from the target cells by internal expression of sialidase.

• Growth curve of PAO1 mearument and data analyzation.
• OD measurement and cell culture medium M9 preparation

• Study and measurement of patients' blood samples.
• Colloection and analyzation of data through SPSS.