NRP2: Two Sides of the Same Blade in Cancer

Authors

• Negin Ziamiavaghi, Virginia Commonwealth University

Original Publication Date

2026

Document Type

Presentation

Comments

12th Annual VCU 3MT® Competition, held on October 9, 2026.

Abstract

Chemotherapy often spares a resilient fraction of prostate cancer cells, leading to recurrence and high mortality. This research investigates Neuropilin-2 (NRP2) isoforms, specifically Neuropilin-2A and Neuropilin-2B, to uncover survival mechanisms. Experiments demonstrate that cancer cells expressing Neuropilin-2B exhibit superior survival and recovery post-chemotherapy. Crucially, deleting 2B's intracellular tail impairs recovery, suggesting it acts as a molecular docking station for survival signaling. Identifying and targeting these tail-binding interactions offers a novel strategy to block post-treatment relapse in advanced prostate cancer.

Accessibility Note

Content is digitally accessible 2026

Transcription

From the School of Medicine, Nigen Zia, NRP2: Two Sides of the Same Blade in Cancer. Their advisor is Dr. Kaustubh Datta. In treating a tumor with chemotherapy, most of the cancer cells die. But if you survive, they stay quiet, recover, and often come back stronger and harder to treat. And this is one of the biggest problems in advanced prostate cancer. This year 36,000 men will die from it. My research asks a simple question. Why do some cancer cells survive treatment? One suspect is a protein called Neuropilin-2. We know that aggressive prostate cancers have high levels of Neuropilin-2 and low survivals. But when I started looking more closely, I found out that Neuropilin is not just one protein. It has two versions, 2A and 2B. I like to think of them as twins. They come from the same gene and they almost look identical from outside, but they have one big difference. Their tails, the part that goes inside the cells, are different. And in biology, a different tail can mean a completely different message. So I started asking myself, is one twin helping cancer cells survive better to test this I genetically changed prostate cancer cells so that they would either express 2A or 2B then I gave them the same chemotherapy the result was interesting cells with 2b survived better my next question was can these cancer cells recover after treatment so I treated the cancer cells with chemotherapy for only 24 hours, removed the drug, and gave the cells time to recover. Then I compared 2B with a version that I deleted its tail. The difference was striking. Cells with 2B recovered strongly, but the no-tail version recovered poorly. This told me that 2B tail is giving its survival advantages. But what is so special about this tail? My hypothesis is that 2B's tail is like acting like a docking station. Inside the cancer cells it is binding to other molecules and sending survival signals. My next step is to find those molecules. And why is this important? Because if I can find those molecules and block their binding to that docking station, I can stop cancer cells from coming back after treatment. Thank you.

Rights

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