The ‘RNA-Binding Ome’: Future Implications for Chemotherapeutic Efficacy

Jonathan R Brodya Jefferson Pancreas, Biliary and Related Cancer Center, Thomas Jefferson University, 1015 Walnut Street, Curtis 611A, Philadelphia, PA19107, USA. [email protected]Correspondence[email protected]
View further author information

Agnieszka K Witkiewiczb Department of Pathology, Thomas Jefferson University, 285 D Main Building, 132 S 10th Street, Philadelphia, PA19107, USAView further author information

Charles J Yeoc Department of Surgery, Thomas Jefferson University, 1015 Walnut Street, 620 CurtisPhiladelphia, PA19107, USAView further author information

Myriam Gorosped LCMB, National Institute on Aging – Intramural Research Program, National Institutes of Health (NIA-IRP, NIH), Biomedical Research Center, 251 Bayview Blvd, Baltimore, MD21224, USAView further author information

Judith C Keene University of Medicine and Dentistry, New Jersey – Robert Wood Johnson Medical School, 401 Haddon Ave, Rm 170, Camden, NJ08103, USAView further author information

Figures & data

Figure 1. HuR regulation of the commonly used chemotherapeutic used against pancreatic cancer, gemcitabine.

Step 1: Gemcitabine is infused as a prodrug; Step 2: Gemcitabine induces the cytoplasmic accumulation of HuR–dCK mRNA complexes (as well as the accumulation of HuR associated to other mRNAs, yet to be identified); Step 3: Activated and increased HuR enhances the expression of dCK (the enzyme that activates the prodrug gemcitabine), and proteins encoded by other HuR target mRNAs; Step 4: Gemcitabine (prodrug) is metabolized into active metabolites in cancer cells, in turn inhibiting the elongation of the DNA chain and causing cell death.

dCK: Deoxycytidine kinase.

Figure 1. HuR regulation of the commonly used chemotherapeutic used against pancreatic cancer, gemcitabine. Step 1: Gemcitabine is infused as a prodrug; Step 2: Gemcitabine induces the cytoplasmic accumulation of HuR–dCK mRNA complexes (as well as the accumulation of HuR associated to other mRNAs, yet to be identified); Step 3: Activated and increased HuR enhances the expression of dCK (the enzyme that activates the prodrug gemcitabine), and proteins encoded by other HuR target mRNAs; Step 4: Gemcitabine (prodrug) is metabolized into active metabolites in cancer cells, in turn inhibiting the elongation of the DNA chain and causing cell death.dCK: Deoxycytidine kinase.

Reprints and Corporate Permissions

Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?

To request a reprint or corporate permissions for this article, please click on the relevant link below:

Order Reprints Request Corporate Permissions

Academic Permissions

Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?

Obtain permissions instantly via Rightslink by clicking on the button below:

Request Academic Permissions

If you are unable to obtain permissions via Rightslink, please complete and submit this Permissions form. For more information, please visit our Permissions help page.

The ‘RNA-Binding Ome’: Future Implications for Chemotherapeutic Efficacy

Information for

Open access

Opportunities

Help and information

Your download is now in progress and you may close this window

Login or register to access this feature

The ‘RNA-Binding Ome’: Future Implications for Chemotherapeutic Efficacy

Figures & data

Reprints and Corporate Permissions

Academic Permissions

Related research

To cite this article:

Download citation

Information for

Open access

Opportunities

Help and information

Keep up to date