Chia-Hung Sun1
Taipei City Hospital, Taipei
Title: Stimulation of 17α-ethynylestradiol and 4-nonylphenol on lung adenocarcinoma cell proliferation via xenoestrogenic way
Biography
Chia-Hung Sun is a chest medicine doctor and also a Ph.D. student in the Department and Graduate Institute of Physiology, National Yang-Ming University. His investigation is based on clinical and basic medical studies. Lung cancer is the major research object in his Ph.D. program.
Abstract
Statement of the Problem: Lung cancer is one of the major causes of cancer death in the world. In addition to smoking, estrogen is considered to play an important role in the lung cancer development because there are still many non-smokers suffer from lung cancer, especially women. In the environment, some metabolites and waste that similar to human estrogen structurally and functionally are called xenoestrogens. 17α-Ethynylestradiol (EE2) is used as an oral contraceptive and then released into wastewater after being utilized. Moreover, 4-nonylphenol (NP) which is found in the petrochemical products and air pollutants also reveals estrogenic activity. Methodology & Theoretical Orientation: In our experiment, 17β-estradiol (E2), EE2, and NP are administered to stimulate the male (A549) and female lung adenocarcinoma cells (H1435). Findings: The results demonstrate that EE2 and NP stimulate A549 and H1435 cell proliferation in a dose- and time-dependent manner. Both estrogen receptors α and β are simultaneously activated and up-regulated by epidermal growth factor receptor and extracellular signal-regulated kinase. Conclusion & Significance: This is the first study to report that EE2 and NP exert an ecotoxic effect to stimulate the proliferation of both male and female lung cancer cells. The new challenges of environmental estrogens to lung cancer deserve further investigation in the future.
Jou-Chun Chou1
China Medical University Hospital, China
Title: Prolactin activation of JAK2/STAT3 signaling pathway through GHR in NSCLC
Biography
Ms. Jou-Chun Chou is a Ph.D. student in the Department of Life Sciences, National Chung Hsing University, Taichung, Taiwan, ROC. Her major is to study the effect and action mechanism of prolactin on the proliferation of human non-small cell lung cancer under the advices of Dr. H. Lin and Dr. P. S. Wang.
Abstract
It is known that PRL could lead breast and prostate cancer progressions. Recent reports point out the concentration of serum PRL in Non Small Cell Lung Cancer (NSCLC) patients are significantly higher than that in healthy people. The patients with higher concentration of serum PRL have lower survival rate than that in patients with normal level of serum PRL. PRL receptor (PRLR) expression level, however, is not related to patients’ survival rate. It is unclear whether PRL promotes lung cancer progression. Meanwhile, the action mechanism of PRL in the proliferation of lung cancer is still unknown. Cells were seeded in 96-well plates with complete medium. After 24 h of plating, cells were serum starved for 16 h and then treated with PRL. MTT assay was applied for cell proliferation. The protein levels of JAK2/STAT3 and VEGF were determined by western blot. The mRNA level was measured by quantitative real time polymerase chain reaction. Our data show that PRL promoted cell proliferation in NSCLC cells. Expressed growth hormone receptor (GHR), not PRLR, was observed in all NSCLC cell lines. Increased expressions of p-JAK2 and p-STAT3 were found in cells treated with PRL. Treatment of PRL also increased STAT3-regulated downstream gene VEGF protein and mRNA expressions. In contrast, the protein expression of p-JAK2 was decreased after inhibition of GHR. PRL activates GHR downstream signaling pathway of JAK2/STAT3. Activated STAT3 is translocated to nucleus and increases downstream gene VEGF activity. PRL promotes cell proliferation and VEGF expression in NSCLC cells.