Feng Yuan Yuan (馮圓媛)
Feng Yuan Yuan (馮圓媛)
MS in Pharmacology, NTU 2019
Yuan-Yuan knew that she was formed by God's hands, dreamed up in his heart, and placed in this world for a purpose. The composition of Yuan-Yuan consists 70% of sensibility and 30% of rationality, so she has chosen something that advocates the scientific thoughts and spirit as her major, like pharmacy and biology-related researches, trying to balance herself. However, the HBx protein (Hepatitis B X protein) played circles around her during the whole master’s degree phase that she sometimes felt depressed and forgot that the universe created by God is too amazing to be easily uncovered. Yuan-Yuan definitely loves transferring concepts of something meaningful, such as critical scientific knowledge and precious feelings, to those who are willing to listen, and she also enjoys receiving them from her beloved ones. Currently, the biggest challenge for her is to decide whether applying the Ph.D. program is the best choice for her. Perhaps someday she could become an inspirational teacher like Dr. Tsai.
To uncover the mystery that whether HBx-induced events are calcium dependent.
HBx(Hepatitis B virus X) is a viral protein encoded by HBV(Hepatitis B virus), and it is reported to be highly related to the incidence of HBV-related HCC(Hepatocellular carcinoma). HCC takes the greatest part of hepatic cancer without effective ways to reach the cure, unfortunately. Due to the relationship between HBx and its abilities to promote HBV replication and transcription, and the phenomena indicated by previous reports that the homolog of anti-apoptotic protein Bcl-2, CED-9, was targeted by HBx to elevate intracellular calcium signaling and alteration of cytosolic calcium was essential for HBV replication mediated by HBx, we came up with an idea that perhaps HBx may lead to HCC by regulating calcium signaling. To address our question, we divided it into two parts, to clarify HBx-induced calcium signaling and to find out whether HBx-related effects are calcium-dependent. And my project focused on the second one.
As for now, we found that HBx significantly induced cell count reduction and tried to figure out its association to calcium signaling. Besides, we used EGF(epidermal growth factor) as a positive control to examine cell count and surprisingly found that HBx seemed to reduce the effect of EGF-related cell number addition on two cell lines, HepG2 and FL83B. We have tried to explore whether the effect of HBx on cell number is dependent on EGFR signaling, and the association between EGFR activation and calcium signaling made us to examine HBx effect on EGFR expression and its downstream signaling pathway. The main result revealed that HBx enhanced the signal of phosphorylated ERK and shortened the duration of phosphorylated AKT signaling. Currently, we are working on using GCaMP6s as a calcium indicator to compare calcium signaling change on HBx and control group after EGF treatment.