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Qi Chen, PhD

Associate Professor
Ph.D., Department of Biochemistry, Sun Yet-sen University, China 2003
Postdoctoral Fellow, NIDDK / NIH , 2008

Basic and translational research in cancer medicine, cancer drug development and mechanism studies with small molecules, with current focus on cancer epithelial-mesenchymal transition and cancer stem cells.

Enrichment of stem-like cancer cells (CSCs) in pancreatic cancer has been proposed to root the poor prognosis and treatment outcomes of this disease. The presence of CSCs is highly associated with cancer cell epithelial-mesenchymal transition (EMT) that contributes to chemo resistant tumors prone to metastasis and recurrence. It is well accepted that EMT is an important initial step during the complicated process of cancer cell dissemination and metastasis. Therefore, inhibiting cancer cell EMT and CSC has emerged to be an important strategy for ultimate elimination of cancer cell populations.

Our lab currently have 3 projects centered on this focus.

1) Investigating the role of HuR in EMT and CSC. HuR is a RNA binding protein, and is increasingly recognized as a pivotal factor in cancer-related gene expression. HuR levels have been found to be abundant in pancreatic cancer as well as in many other types of cancers. Typically, HuR binds to 3'-untranslated regions (3'-UTRs) of target mRNAs promoting their stabilization and overexpression. Through regulation of mRNA turnover and translation, HuR contributes to many cellular processes including cell survival, proliferation, angiogenesis, anti-apoptosis, as well as reduced immune recognition. In addition, HuR enhances cancer cell invasion and metastasis by stabilizing mRNAs of MMPs, uPA, and Snail. However, the mechanisms that HuR could be involved in cancer cell EMT have not been elucidated. Understanding the mechanism of HuR's involvement in cancer cell EMT will not only add to our knowledge a new level of regulation of EMT, but also provide a novel approach for design of drugs targeting EMT and CSCs.

2) Investigating the use of high dose intravenous ascorbate (vitamin C, ascorbic acid) as a cancer treatment. High dose of intravenous ascorbate (IVC) is a popular treatment for cancer in the world of complementary and alternative medicine (CAM), with profound safety and anicdotal clinical benefits. We have made the fundamental discovery that intravenous administration of ascorbate by passes its physiological "tight control" of obsoption for oral doses, reaches concentrations in millimolar in the body, and exerts a pro-oxidant action, in contrast to its normal anti-oxidant role, by generating ascorbate radical and hydrogen peroxide (H2O2) to tissues, with minimal formation of ROS in blood. The pro-oxidant action of ascorbate selectively kills cancer cells but spares normal cells, by mechanisms not understood yet. A number of animal studies all over the world have confimed our discovery that ascorbate treatment reduced tumor growth of various cancers. Partially based on our studies, there have been >10 early phase clinical trials all over the world elucidating safety and pharmacokinetic characteristics of IVC. We have had two Phase I/IIa studies in ovarian cancer and pancreatic cancer, respectively, both proved low toxicity, high tolerability, safety, and potential benefit in patients. We are now planning a Phase II study in ovarian cancer to identify clinical benefits, to further investigate the mechanisms of actions, and to find biomarkers for patient selection.

3) Identifying novel compounds that inhibit cancer cell EMT. A high-throughput screening project was conducted identifying small molecules that inhibit pancreatic cancer cell EMT. Validation and further mechanistic and efficacy studies of positive hits have the potential towards discovery of novel drug leads that comprehensively inhibit pancreatic cancer metastasis, recurrence, and overcome drug resistance.


Selected Publications:

Ma Y, Chen P, Drisko J, Godwin AG, Chen Q.  Pharmacologic Ascorbate Induces “BRCAness” and Enhances Effects of Poly(ADP-Ribose) Polymerase Inhibitors against BRCA1/2 Wild-type Ovarian Cancer. Oncology Letters. 2019.

Dong R, Chen P, Chen Q. Inhibition of Pancreatic Cancer Stem Cells by Rauwolfia vomitoria extract. Oncology Reports. 2018, 40: 3144-54.

Polireddy K, Dong R, Reed G, Yu J, Chen P, Williamson S, Violet PC, Pessetto Z, Godwin AK, Fan F, Levine M, Drisko JA, Chen Q. High Dose Parenteral Ascorbate Inhibited Pancreatic Cancer Growth and Metastasis: Mechanisms and a Phase I/II Study.  Sci Rep. 2017, 7:17188. (One of the top 100 reviewed articles of the journal in 2017).

Ma E, Chen P, Wilkins HM, Wang T, Russell HS, Chen Q. Pharmacologic ascorbate induces neuroblastoma cell death by hydrogen peroxide mediated DNA damage and reduction in cancer cell glycolysis. Free Radic Biol Med. 2017; 113: 36-47.

Polireddy K, Dong R, McDonald PR, Wang T, Luke B, Chen P, Broward M, Roy A, Chen Q. Targeting epithelial-mesenchymal transition for identification of inhibitors for pancreatic cancer cell invasion and tumor spheres formation. PLoS One. 2016 Oct 20;11(10):e0164811.

Ma Y, Chapman J, Levine M, Polireddy K, Drisko J, Chen Q. High-dose parenteral ascorbate enchanced chemosensitivity of ovarian cancer and reduced toxicity of chemotherapy. Science Translational Medicine. 2014, 6, 222ra18. (Featured with a commentary article)

Yu J, Chen Q. Antitumor activities of Rauwolfia vomitoria extract and potentiation of gemcitabine effects against pancreatic cancer. Integrative Cancer Therapies. 2014, 13 (3): 217-25.

Chen P, Zhang Y, Polireddy K, Chen Q. The tumor-suppressing activity of the prenyl diphosphate synthase subunit 2 gene in lung cancer cells. Anti-Cancer Drugs. 2014, 25(7): 790-8.

Yu J, Drisko J, Chen Q. Inhibition of pancreatic cancer and potentiation of gemcitabine effects by extract of Pao Pereira. Oncology Report. 2013, 30 (1): 149-56.

Chen P, Yu J, Knecht J, Chen Q. Decrease of PDSS2 expression, a novel tumor suppressor, in non-small cell lung cancer. Cancer Epidemiology. 2013; 37: 166-71.

Chen P, Yu J, Chalmers B, Drisko J, Yang J, Li BY,  Chen Q. Pharmacological Ascorbate Induces Cytotoxicity in Prostate Cancer Cells through ATP Depletion and Induction of Autophagy. Anti-Cancer Drugs; 2012; 23(4):437-44.

Espey MG, Chen P, Chalmers B, Drisko J, Sun AY, Levine M, Chen Q. Pharmacologic ascorbate synergizes with gemcitabine in pre-clinical models of pancreatic cancer. Free Radic Biol Med. 2011; 50(11): 1610-9.

Chen P, Stone J, Sullivan G, Drisko J, Chen Q. Supplementary glutathione counteracts with pharmacologic ascorbate in pre-clinical cancer models. Free Radic Biol Med. 2011; 51(3):681

Chen Q., Espey M.G., Sun A.Y., Pooput C., Kirk K.L., Krishna M.C., Khosh D.B., Drisko J.A., Levine M.. Pharmacologic doses of ascorbate act as a pro-oxidant and decrease growth of aggressive tumor xenografts in mice. Proc Natl Acad Sci USA. 2008; 105 (32): 11105-9. (Featured in PANS paper of the week)

Chen Q., Espey M.G., Sun A.Y., Lee J.H., Cherukuri M.K., Shacter E, Choyke P.L., Pooput C., Kirk K.L., Buettner G.R., Levine M. Ascorbate in pharmacologic concentrations selectively generates ascorbate radical and hydrogen peroxide in extracellular fluid in vivo. Proc Natl Acad Sci USA. 2007; 104(21): 8749-54.

Chen Q., Espey M.G., Krishna M.C., Mitchell J.B., Corpe C.P., Buettner G.R., Shacter E., Levine M. Ascorbic acid at pharmacologic concentrations selectively kills cancer cells: ascorbic acid as a pro-drug for hydrogen peroxide delivery to tissues. Proc Natl Acad Sci USA. 2005; 102(38): 13604-9. (Featured in PANS paper of the week)


Last modified: Jul 23, 2019

Qi Chen, Ph.D.


Qi Chen, PhD
Associate Professor

G001 Wahl East; MS-1018
3901 Rainbow Blvd.
Kansas City, KS 66160

P: (913) 588-3690
F: (913) 588-0012