First Person is a series of interviews with the first authors of a selection of papers published in Journal of Cell Science, helping early-career researchers promote themselves alongside their papers. Varisa Pongrakhananon is the first author on ‘Loss of CAMSAP3 promotes EMT via the modification of microtubule–Akt machinery’, published in Journal of Cell Science. Varisa is an Assistant Professor at Chulalongkorn University, Bangkok, Thailand, investigating the role of CAMSAP proteins on cancer cell biology.

Varisa Pongrakhananon

How would you explain the main findings of your paper in lay terms?

We investigate the role of CAMSAP3 on lung cancer cell migration. Similar to the bones in our body, microtubules also function to maintain structure, but inside the cell. Microtubules, which are rod-like structures, contain two ends: a minus-end, which is a microtubule nucleation site, and a plus-end, which is an elongation site. Microtubules are dynamic structures that can be shortened or extended in response to cellular activity. It has been reported that CAMSAP3, a microtubule minus-end-binding protein, regulates these microtubule behaviors, as well as cell morphology. Our findings show that lung cancer cells that lack CAMSAP3 have a higher rate of movement, an important characteristic of metastatic cancer cells. We further found that microtubule acetylation and Akt play a role in this phenomenon. This study highlights the important functions of CAMSAP3 on lung cancer cell behavior, which might be a target for drug research and development in the future.

Were there any specific challenges associated with this project? If so, how did you overcome them?

This work came out of previous research on the function of CAMSAP3 in neuronal development. Once we found that CAMSAP3-knockout cells exhibit rapid cell movement via an epithelial-mesenchymal transition (EMT)-like mechanism, another challenge was determining how CAMSAP3 regulates the EMT process. There were fewer clues showing the relationship between CAMSAP3 and cell migration. We proposed many hypotheses, and tried hard to test all of them. We kept getting negative results or found our hypotheses to be wrong many times, but we learned from this. We eventually found the key molecular mechanism underlying this regulation. We believe that all of our efforts led to interesting results, so we obtained much data, besides those for the main project, that could be extended to further work.

“We kept getting negative results or found our hypotheses to be wrong many times, but we learned from this.”

When doing the research, did you have a particular result or ‘eureka’ moment that has stuck with you?

I remember that moment very well, after working hard to perform many experiments to find out how CAMSAP3 regulates EMT. I was disappointed many times. One day, I conducted an immunofluorescence experiment and surprisingly found that the signal of phosphorylated Akt was intensified. At first, I did not believe it because it could have been the wrong signal. So I repeated the experiment many times and got consistent results. I was very excited, and that moment is my ‘eureka’.

Why did you choose Journal of Cell Science for your paper?

Journal of Cell Science has a great reputation for publishing a lot of ‘eureka’ works in cell biology. The articles in the journal are high quality and have many citations. Furthermore, the review process was impressive, and the reviewers and editor provided valuable comments that helped us improve this work, and could also help with our future work.

Have you had any significant mentors who have helped you beyond supervision in the lab?

This work could not be done without my great mentor, Professor Masatoshi Takeichi. His guidance and suggestions always inspire me to do science, and energize me when I have got stuck in the experiments. Professor Takeichi always finds the fascinating side of my data that I have never noticed, which is very important for the research.

I would like to thank Dr Ubonthip Nimmannit and Dr Pithi Chanvorachote, who were my supervisors when I was a PhD student. They are the first people who introduced me to cell-based experiments. Without them, I would not be where I am today.

His-taggedCAMSAP3 (green) decorated on microtubules (red) in CAMSAP3-overexpressing H460 cells.

His-taggedCAMSAP3 (green) decorated on microtubules (red) in CAMSAP3-overexpressing H460 cells.

What motivated you to pursue a career in science, and what have been the most interesting moments on the path that led you to where you are now?

I was interviewed by Professor Masatoshi Takeichi when I applied for a post-doctoral fellowship in his laboratory. He asked me one question: “why you like to do science?”. At that time, I had no idea, so I just answered that I could establish new knowledge and present it to the world. It is quite a general and common answer. But he told me that he is always excited with results every time, especially if he gets surprising data. And now, I totally agree with his answer. He is a great scientist and mentor. I could say that he is a role model in science. That why I keep doing research: to reveal the mysteries of science.

What's next for you?

Research is a part of my life. Many people want do something that helps them find their worth. This is also true in my case. I will keep doing research to find therapeutic approaches to treat cancer. I hope I can establish a breakthrough in the future.

Tell us something interesting about yourself that wouldn't be on your CV

Even though I love to do science, sometimes if I am having trouble in the lab, I feel nervous and stressed, so I will take a short trip to visit new places and do new things that give me a fresh perspective. Then I can come back to the lab and do it better.

Varisa Pongrakhananon's contact details: Department of Pharmacology and Physiology, Faculty of Pharmaceutical Sciences, Chulalongkorn University, Bangkok, Thailand.

E-mail: Varisa.p@pharm.chula.ac.th

Pongrakhananon
,
V.
,
Wattanathamsan
,
O.
,
Takeichi
,
M.
,
Chetprayoon
,
P.
and
Chanvorachote
,
P.
(
2018
).
Loss of CAMSAP3 promotes EMT via the modification of microtubule-Akt machinery
.
J. Cell Sci.
131
,
jcs216168
.