Search

Your search keyword '"Sasabe, Eri"' showing total 135 results
Start Over Author "Sasabe, Eri"
Sorry, I don't understand your search. ×
135 results on '"Sasabe, Eri"'

4. The involvement of epidermal growth factor receptor/protein kinase B signaling in the tumor intrinsic PD‐L1‐induced malignant potential of oral squamous cell carcinoma.

Author

Sasabe, Eri, Tomomura, Ayumi, and Yamamoto, Tetsuya

Subjects
*PROTEIN kinase B, *EPIDERMAL growth factor receptors, *ERLOTINIB, *SQUAMOUS cell carcinoma, *SMALL interfering RNA
Abstract

Background: Various antigen‐presenting cells and tumor cells‐expressing PD‐L1 inhibits antitumor immune responses in the tumor microenvironment. Recently, numerous studies have shown that tumor cell intrinsic PD‐L1 also plays important roles in tumor growth and progression. On the other hand, oral squamous cell carcinoma (OSCC) cells overexpress epidermal growth factor receptor (EGFR) and EGFR signal pathway exacerbates tumor progression. Therefore, this study assessed whether tumor‐intrinsic PD‐L1 facilitates malignant potential of OSCC cells through regulation of EGFR signaling. Methods: Two OSCC cell lines, SAS and HSC‐3, were transfected with PD‐L1 and EGFR‐specific small interfering RNA (siRNA). Influences of PD‐L1 knockdown on malignant potentials of OSCC cells were examined by Cell Counting kit‐8 assay, transwell assay, sphere formation assay, flow cytometry, and Western blot. Effects of PD‐L1 and EGFR knockdown on each expression were examined by quantitative real‐time PCR (qRT‐PCR), Western blot, and flow cytometry. Results: Transfection of an PD‐L1‐siRNA into OSCC cells decreased the abilities of proliferation, stemness, and mobility of these cells significantly. PD‐L1 knockdown also decreased EGFR expression through the promotion of proteasome‐ and lysosome‐mediated degradation and following activation of the EGFR/protekin kinase B (AKT) signal pathway. Meanwhile, EGFR knockdown did not influence PD‐L1 expression in SAS and HSC‐3 cells, but treatment with a recombinant human EGF induced its expression. Treatment with erlotinib and cetuximab suppressed rhEGF‐induced PD‐L1 expression and localization in the cellular membrane of both OSCC cells. Conclusion: OSCC cells‐expressing PD‐L1 induced by EGF stimulation may promote malignancy intrinsically via the activation of the EGFR/AKT signaling cascade. [ABSTRACT FROM AUTHOR]

Published
2024
Full Text
View/download PDF

20. Gene therapy with SOCS1 induces potent preclinical antitumor activities in oral squamous cell carcinoma.

Author

Nakatani, Kie, Serada, Satoshi, Fujimoto, Minoru, Obata, Kengo, Ohkawara, Tomoharu, Sasabe, Eri, Yamamoto, Tetsuya, and Naka, Tetsuji

Abstract

Background: Constitutive activation of STAT3 promotes oncogenesis and growth of oral squamous cell carcinoma (OSCC). We investigated the mechanism of action of suppressor of cytokine signaling 1 (SOCS1), an endogenous inhibitor of JAK, as gene therapy for OSCC. Methods: Antitumor effect of SOCS1 was compared to JAK inhibitor I by cell proliferation assay, cell cycle analysis, and apoptosis analysis in vitro. In addition, antitumor effect was evaluated using xenograft mouse models in vivo. Results: JAK inhibitor I inhibited the proliferation of KOSC2 cl3‐43 or T3M‐1 clone2 OSCC cell lines in vitro. While JAK inhibitor I arrested both cell lines at the G2/M phase, induction of apoptosis was observed in T3M‐1 clone2 cells, but not KOSC2‐cl3‐43 cells. An adenoviral vector expressing SOCS1 (AdSOCS1) significantly decreased the proliferation of both OSCC cell lines and induced G2/M phase cell cycle arrest and apoptosis, suggesting that induction of apoptosis of KOSC2 cl3‐43 cells by AdSOCS1 is regulated by the JAK/STAT independent pathway. Overexpression of SOCS1 inhibited activation of the JAK/STAT and p44/42 MAPK pathways, while JAK inhibitor I inhibited activation of the JAK/STAT pathway only. Consistently, expression of Mcl‐1 was decreased by overexpression of SOCS1, but not JAK inhibitor I. Additionally, KOSC2 cl3‐43 or T3M‐1 clone2 OSCC cells were subcutaneously implanted in the flanks of two xenograft mouse models. As compared to a control adenovirus vector (AdLacZ), intratumor injection of AdSOCS1 significantly decreased the tumor volume and induced apoptosis in vivo. Conclusion: SOCS1 gene therapy may be a beneficial approach for the treatment of OSCC. [ABSTRACT FROM AUTHOR]

Published
2022
Full Text
View/download PDF

21. Epidermal growth factor/epidermal growth factor receptor signaling blockage inhibits tumor cell‐derived exosome uptake by oral squamous cell carcinoma through macropinocytosis.

Author

Sasabe, Eri, Tomomura, Ayumi, Liu, Hangyu, Sento, Shinya, Kitamura, Naoya, and Yamamoto, Tetsuya

Abstract

Various cell types secrete exosomes into their surrounding extracellular space, which consequently affect the function and activity of recipient cells. Numerous studies have showed that tumor cell‐derived exosomes play important roles in tumor growth and progression. Although a variety of endocytic pathways are reportedly involved in the cellular uptake of exosomes, detailed mechanisms remain unknown. The present study demonstrated that treatment with recombinant epidermal growth factor (EGF) time‐ and dose‐dependently promoted cellular uptake of oral squamous cell carcinoma (OSCC) cell‐derived exosomes into OSCC cells themselves. Conversely, EGF receptor (EGFR) knockdown and treatment with EGFR inhibitors, including erlotinib and cetuximab, abrogated OSCC cell uptake of exosomes. The macropinocytosis inhibitor 5‐(N‐ethyl‐N‐isopropyl) amiloride (EIPA) blocked the effects of active EGF/EGFR signaling on uptake of OSCC cell‐derived exosomes. These EGFR inhibitors also suppressed OSCC cell‐derived exosome‐induced proliferation, migration, invasion, stemness, and chemoresistance of OSCC cells. Taken together, the data presented herein suggest that EGFR inhibitors might inhibit the malignant potential of OSCC cells through direct inhibition of not only EGFR downstream signaling pathway but also cellular uptake of OSCC cell‐derived exosomes through macropinocytosis. [ABSTRACT FROM AUTHOR]

Published
2022
Full Text
View/download PDF

38. Mucinous Cystadenoma in the Upper Lip

Author

Yamada, Tomohiro, primary, Takahashi, Mayu, additional, Matsumoto, Manabu, additional, Toi, Makoto, additional, Ohno, Seiji, additional, Kitamura, Naoya, additional, Sasabe, Eri, additional, and Yamamoto, Tetsuya, additional

Published
2013
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results