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15 results on '"Kibe, Shin"'

2. Targeting Pin1 renders pancreatic cancer eradicable by synergizing with immunochemotherapy

Author

Koikawa, Kazuhiro, Kibe, Shin, Suizu, Futoshi, Sekino, Nobufumi, Kim, Nami, Manz, Theresa D., Pinch, Benika J., Akshinthala, Dipikaa, Verma, Ana, Gaglia, Giorgio, Nezu, Yutaka, Ke, Shizhong, Qiu, Chenxi, Ohuchida, Kenoki, Oda, Yoshinao, Lee, Tae Ho, Wegiel, Babara, Clohessy, John G., London, Nir, Santagata, Sandro, Wulf, Gerburg M., Hidalgo, Manuel, Muthuswamy, Senthil K., Nakamura, Masafumi, Gray, Nathanael S., Zhou, Xiao Zhen, and Lu, Kun Ping

Published
2021
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3. Sulfopin is a covalent inhibitor of Pin1 that blocks Myc-driven tumors in vivo

Author

Dubiella, Christian, Pinch, Benika J., Koikawa, Kazuhiro, Zaidman, Daniel, Poon, Evon, Manz, Theresa D., Nabet, Behnam, He, Shuning, Resnick, Efrat, Rogel, Adi, Langer, Ellen M., Daniel, Colin J., Seo, Hyuk-Soo, Chen, Ying, Adelmant, Guillaume, Sharifzadeh, Shabnam, Ficarro, Scott B., Jamin, Yann, Martins da Costa, Barbara, Zimmerman, Mark W., Lian, Xiaolan, Kibe, Shin, Kozono, Shingo, Doctor, Zainab M., Browne, Christopher M., Yang, Annan, Stoler-Barak, Liat, Shah, Richa B., Vangos, Nicholas E., Geffken, Ezekiel A., Oren, Roni, Koide, Eriko, Sidi, Samuel, Shulman, Ziv, Wang, Chu, Marto, Jarrod A., Dhe-Paganon, Sirano, Look, Thomas, Zhou, Xiao Zhen, Lu, Kun Ping, Sears, Rosalie C., Chesler, Louis, Gray, Nathanael S., and London, Nir

Published
2021
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4. Identification of a potent and selective covalent Pin1 inhibitor

Author

Pinch, Benika J., Doctor, Zainab M., Nabet, Behnam, Browne, Christopher M., Seo, Hyuk-Soo, Mohardt, Mikaela L., Kozono, Shingo, Lian, Xiaolan, Manz, Theresa D., Chun, Yujin, Kibe, Shin, Zaidman, Daniel, Daitchman, Dina, Yeoh, Zoe C., Vangos, Nicholas E., Geffken, Ezekiel A., Tan, Li, Ficarro, Scott B., London, Nir, Marto, Jarrod A., Buratowski, Stephen, Dhe-Paganon, Sirano, Zhou, Xiao Zhen, Lu, Kun Ping, and Gray, Nathanael S.

Published
2020
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7. Pancreatic stellate cells reorganize matrix components and lead pancreatic cancer invasion via the function of Endo180

Author

Koikawa, Kazuhiro, Ohuchida, Kenoki, Takesue, Shin, Ando, Yohei, Kibe, Shin, Nakayama, Hiromichi, Endo, Sho, Abe, Toshiya, Okumura, Takashi, Horioka, Kohei, Sada, Masafumi, Iwamoto, Chika, Moriyama, Taiki, Nakata, Kohei, Miyasaka, Yoshihiro, Ohuchida, Riichi, Manabe, Tatsuya, Ohtsuka, Takao, Nagai, Eishi, Mizumoto, Kazuhiro, Hashizume, Makoto, and Nakamura, Masafumi

Published
2018
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12. Neutrophil extracellular traps promote liver micrometastasis in pancreatic ductal adenocarcinoma via the activation of cancer-associated fibroblasts.

Author

Takesue, Shin, Ohuchida, Kenoki, Shinkawa, Tomohiko, Otsubo, Yoshiki, Matsumoto, Sokichi, Sagara, Akiko, Yonenaga, Akiko, Ando, Yohei, Kibe, Shin, Nakayama, Hiromichi, Iwamoto, Chika, Shindo, Koji, Moriyama, Taiki, Nakata, Kohei, Miyasaka, Yoshihiro, Ohtsuka, Takao, Toma, Hiroki, Tominaga, Yohei, Mizumoto, Kazuhiro, and Hashizume, Makoto

Published
2020
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13. Necroptosis in pancreatic cancer promotes cancer cell migration and invasion by release of CXCL5.

Author

Ando, Yohei, Ohuchida, Kenoki, Otsubo, Yoshiki, Kibe, Shin, Takesue, Shin, Abe, Toshiya, Iwamoto, Chika, Shindo, Koji, Moriyama, Taiki, Nakata, Kohei, Miyasaka, Yoshihiro, Ohtsuka, Takao, Oda, Yoshinao, and Nakamura, Masafumi

Subjects
PANCREATIC cancer, APOPTOSIS, WESTERN immunoblotting, PROTEIN microarrays, CANCER cells, CANCER cell migration, CELL migration inhibition
Abstract

Background: Necroptosis is a form of programmed cell death that is accompanied by release of intracellular contents, and reportedly contributes to various diseases. Here, we investigate the significance of necroptosis in pancreatic cancer. Methods: We used immunohistochemistry and western blot analysis to evaluate expression of the key mediators of necroptosis—receptor-interacting serine/threonine protein kinase 3 (RIP3) and mixed lineage kinase domain-like (MLKL)—in human pancreatic cancer. We also tested the effects of conditioned media (CM) from necroptotic cells on pancreatic cancer cells in Transwell migration and Matrigel invasion assays. Protein array analysis was used to investigate possible mediators derived from necroptotic cells. Results: RIP3 and MLKL are highly expressed in human pancreatic cancer tissues compared with normal pancreas. MLKL expression was particularly intense at the tumor invasion front. CM derived from necroptotic cells promoted cancer cell migration and invasion, but not CM derived from apoptotic cells. C-X-C motif chemokine 5 (CXCL5) was upregulated in CM derived from necroptotic cells compared with CM derived from control or apoptotic cells. Moreover, expression of the receptor for CXCL5, C-X-C-motif chemokine receptor-2 (CXCR2), was upregulated in pancreatic cancer cells. Inhibition of CXCR2 suppressed cancer cell migratory and invasive behavior enhanced by necroptosis. Conclusion: These findings indicate that necroptosis at the pancreatic cancer invasion front can promote cancer cell migration and invasion via the CXCL5–CXCR2 axis. [ABSTRACT FROM AUTHOR]

Published
2020
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15. Adipose tissue‐derived stromal cells are sources of cancer‐associated fibroblasts and enhance tumor progression by dense collagen matrix.

Author

Okumura, Takashi, Ohuchida, Kenoki, Kibe, Shin, Iwamoto, Chika, Ando, Yohei, Takesue, Shin, Nakayama, Hiromichi, Abe, Toshiya, Endo, Sho, Koikawa, Kazuhiro, Sada, Masafumi, Horioka, Kohei, Mochidome, Naoki, Arita, Makoto, Moriyama, Taiki, Nakata, Kohei, Miyasaka, Yoshihiro, Ohtsuka, Takao, Mizumoto, Kazuhiro, and Oda, Yoshinao

Abstract

Although recent studies revealed that adipose tissue accelerates pancreatic tumor progression with excessive extracellular matrix, key players for desmoplasia in the adipose microenvironment remains unknown. Here, we investigated the roles of adipose tissue‐derived stromal cells (ASCs) in desmoplastic lesions and tumor progression by in vitro and in vivo experiments. In a three‐dimensional (3‐D) organotypic fat invasion model using visceral fat from CAG‐EGFP mice, GFP‐positive fibroblastic cells infiltrated toward cancer cells. When tumor cells were inoculated into transplanted visceral fat pads in vivo, tumor weights and stromal components were enhanced compared to subcutaneous and orthotopic tumor cells inoculated without fat pads. Expression of αSMA in established human ASCs was lower compared to cancer associated fibroblasts, and the 3‐D collagen matrices produced by ASCs cultured in cancer cell‐conditioned medium changed from loose to dense structures that affected the motility of cancer cells. Microarray analyses revealed upregulation of S100A4 in ASCs, while S100A4‐positive stromal cells were observed at extrapancreatic invasion sites of human pancreatic cancer. The present findings indicate that ASCs are recruited to extrapancreatic invasion sites and produce dense collagen matrices that lead to enhanced tumor progression. Both inhibition of ASCs recruitment and activation could lead to a novel antistromal therapy. What's new? One of the major pathological features of pancreatic ductal adenocarcinoma is excessive stromal involvement, and anti‐stromal therapies are considered promising against this deadly cancer. Here the authors show in a 3D organotypic fat invasion model or in mice specific infiltration of adipose tissue‐derived stromal cells towards cancer cells and dense collagen production leading to enhanced tumor progression in vivo. They speculate that adipose‐derived stromal cells may be new targets in therapy approaches against pancreatic cancer. [ABSTRACT FROM AUTHOR]

Published
2019
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