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Jun 29, 2022

PDF Seminar (2022-06-29)

Date: Wednesday, 29 June 2022

Time: 5:00 p.m. - 6:00 p.m.

Mode: via Zoom

Registration link:

Meeting ID: 955 6757 0030

Password: 685197

5:00 p.m.

Speaker: Dr. Zheng ZENG (Post-doctoral Fellow)
Primary Supervisor: Prof. Jiandong HUANG
Presentation Title: THBS1 drives the synergistic suppression of epithelial ovarian cancer by enterolactone and trabectedin
Abstract: Natural products are effective adjuvant treatments for ovarian cancer with prove antitumor advantages. Enterolactone (ENL), a microbial metabolite of plant lignans, has remarkable suppressive effects on ovarian cancer. The chemotherapeutic agent trabectedin is effective on relapsed ovarian cancer, especially when combined with other therapeutics. Thrombospondin 1(THBS1), a kind of matrix glycoprotein, was downregulated in epithelial ovarian cancer patients but significantly upregulated in the tumour tissue after ENL treatment. ENL and trabectedin could remarkably suppress cancer cells proliferation, migration, and tube formation either separately or in combination. Ectopic expression of THBS1 resulted in a more suppression of tumour growth. Since the anti-angiogenesis and anti-metastasis activities of THBS1 are ascribed to the 3TSR domain of THBS1, an overexpression of THBS1 3TSR further enhanced the antitumor activities of ENL.


5:30 p.m. 

Speaker: Dr. Shibo ZHANG (Post-doctoral Fellow)
Primary Supervisor: Dr. Lydia CHEUNG
Presentation Title: Investigating the function and therapeutic implications of AKTIP loss in ERα-positive breast cancer
Abstract: Estrogen receptor α (ERα) is expressed in >60% of breast cancer cases and is the target of endocrine therapy for ERα-positive breast cancer patients. However, endocrine resistance is a major barrier to effective treatment outcome. Copy number loss of 16q12.2 is frequent in ERα-positive breast tumors. Yet, little is known about the driver genomic alterations in this locus. In this study, we show that loss of AKTIP, a gene on 16q12.2, induced tumorigenic phenotypes specifically in ERα-positive breast cancer cells. Cells with AKTIP loss had an increased ERα protein level and significant enrichment in ERα-associated gene expression profiles. Intriguingly, JAK2-STAT3 signaling was also activated, which represents a potential mechanism of endocrine resistance. Accordingly, JAK2 inhibitor re-sensitized AKTIP-depleted cells towards ERα antagonists. Our findings collectively suggest that AKTIP may serve as a novel biomarker to predict prognosis and guide treatment selection for breast cancer patients.



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