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31 results on '"Cai, Shurui"'

1. Concurrent inhibition of oncogenic and wild-type RAS-GTP for cancer therapy

Author

Holderfield, Matthew, Lee, Bianca J., Jiang, Jingjing, Tomlinson, Aidan, Seamon, Kyle J., Mira, Alessia, Patrucco, Enrico, Goodhart, Grace, Dilly, Julien, Gindin, Yevgeniy, Dinglasan, Nuntana, Wang, Yingyun, Lai, Lick Pui, Cai, Shurui, Jiang, Lingyan, Nasholm, Nicole, Shifrin, Nataliya, Blaj, Cristina, Shah, Harshit, Evans, James W., Montazer, Nilufar, Lai, Oliver, Shi, Jade, Ahler, Ethan, Quintana, Elsa, Chang, Stephanie, Salvador, Anthony, Marquez, Abby, Cregg, Jim, Liu, Yang, Milin, Anthony, Chen, Anqi, Ziv, Tamar Bar, Parsons, Dylan, Knox, John E., Klomp, Jennifer E., Roth, Jennifer, Rees, Matthew, Ronan, Melissa, Cuevas-Navarro, Antonio, Hu, Feng, Lito, Piro, Santamaria, David, Aguirre, Andrew J., Waters, Andrew M., Der, Channing J., Ambrogio, Chiara, Wang, Zhengping, Gill, Adrian L., Koltun, Elena S., Smith, Jacqueline A. M., Wildes, David, and Singh, Mallika

Published
2024
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7. Data from ALDH1A1 Contributes to PARP Inhibitor Resistance via Enhancing DNA Repair in BRCA2−/− Ovarian Cancer Cells

Author

Liu, Lu, primary, Cai, Shurui, primary, Han, Chunhua, primary, Banerjee, Ananya, primary, Wu, Dayong, primary, Cui, Tiantian, primary, Xie, Guozhen, primary, Zhang, Junran, primary, Zhang, Xiaoli, primary, McLaughlin, Eric, primary, Yin, Ming, primary, Backes, Floor J., primary, Chakravarti, Arnab, primary, Zheng, Yanfang, primary, and Wang, Qi-En, primary

Published
2023
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8. Supplementary Tables S1-S2 and Figures S1-S11 from ALDH1A1 Contributes to PARP Inhibitor Resistance via Enhancing DNA Repair in BRCA2−/− Ovarian Cancer Cells

Author

Liu, Lu, primary, Cai, Shurui, primary, Han, Chunhua, primary, Banerjee, Ananya, primary, Wu, Dayong, primary, Cui, Tiantian, primary, Xie, Guozhen, primary, Zhang, Junran, primary, Zhang, Xiaoli, primary, McLaughlin, Eric, primary, Yin, Ming, primary, Backes, Floor J., primary, Chakravarti, Arnab, primary, Zheng, Yanfang, primary, and Wang, Qi-En, primary

Published
2023
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9. Supplementary Data from Inhibition of miR-328–3p Impairs Cancer Stem Cell Function and Prevents Metastasis in Ovarian Cancer

Author

Srivastava, Amit K., primary, Banerjee, Ananya, primary, Cui, Tiantian, primary, Han, Chunhua, primary, Cai, Shurui, primary, Liu, Lu, primary, Wu, Dayong, primary, Cui, Ri, primary, Li, Zaibo, primary, Zhang, Xiaoli, primary, Xie, Guozhen, primary, Selvendiran, Karuppaiyah, primary, Patnaik, Srinivas, primary, Karpf, Adam R., primary, Liu, Jinsong, primary, Cohn, David E., primary, and Wang, Qi-En, primary

Published
2023
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10. Data from Inhibition of miR-328–3p Impairs Cancer Stem Cell Function and Prevents Metastasis in Ovarian Cancer

Author

Srivastava, Amit K., primary, Banerjee, Ananya, primary, Cui, Tiantian, primary, Han, Chunhua, primary, Cai, Shurui, primary, Liu, Lu, primary, Wu, Dayong, primary, Cui, Ri, primary, Li, Zaibo, primary, Zhang, Xiaoli, primary, Xie, Guozhen, primary, Selvendiran, Karuppaiyah, primary, Patnaik, Srinivas, primary, Karpf, Adam R., primary, Liu, Jinsong, primary, Cohn, David E., primary, and Wang, Qi-En, primary

Published
2023
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14. A Novel Estrogen Receptor b Agonist Diminishes Ovarian Cancer Stem Cells via Suppressing the Epithelial-To-Mesenchymal Transition

Author

Banerjee, Ananya, primary, Cai, Shurui, additional, Xie, Guozhen, additional, Li, Na, additional, Bai, Xuetao, additional, Lavudi, Kousalya, additional, Wang, Kevin, additional, Zhang, Xiaoli, additional, Zhang, Junran, additional, Patnaik, Srinivas, additional, Backes, Floor J., additional, Bennett, Chad, additional, and Wang, Qi-En, additional

Published
2022
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15. Micropeptide PACMP inhibition elicits synthetic lethal effects by decreasing CtIP and poly(ADP-ribosyl)ation

Author

Zhang, Chuanchao, primary, Zhou, Bo, additional, Gu, Feng, additional, Liu, Hongmei, additional, Wu, Honglin, additional, Yao, Fuwen, additional, Zheng, Hui, additional, Fu, Hui, additional, Chong, Wei, additional, Cai, Shurui, additional, Huang, Min, additional, Ma, Xiaolu, additional, Guo, Zhifang, additional, Li, Tingting, additional, Deng, Wenyuan, additional, Zheng, Meiwen, additional, Ji, Qiao, additional, Zhao, Yongliang, additional, Ma, Yongjie, additional, Wang, Qi-En, additional, Tang, Tie-Shan, additional, and Guo, Caixia, additional

Published
2022
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16. ERK inactivation enhances stemness of NSCLC cells via promoting Slug-mediated epithelial-to-mesenchymal transition

Author

Cai, Shurui, primary, Li, Na, additional, Bai, Xuetao, additional, Liu, Lu, additional, Banerjee, Ananya, additional, Lavudi, Kousalya, additional, Zhang, Xiaoli, additional, Zhao, Jihe, additional, Venere, Monica, additional, Duan, Wenrui, additional, Zhang, Junran, additional, Welliver, Meng X., additional, He, Kai, additional, and Wang, Qi-En, additional

Published
2022
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18. Discovery of a Bicyclic Peptidyl Pan-Ras Inhibitor

Author

Buyanova, Marina, primary, Cai, Shurui, additional, Cooper, Jahan, additional, Rhodes, Curran, additional, Salim, Heba, additional, Sahni, Ashweta, additional, Upadhyaya, Punit, additional, Yang, Rui, additional, Sarkar, Amar, additional, Li, Na, additional, Wang, Qi-En, additional, and Pei, Dehua, additional

Published
2021
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21. Identification of Rhizospheric Actinomycete Streptomyces lavendulae SPS-33 and the Inhibitory Effect of its Volatile Organic Compounds against Ceratocystis Fimbriata in Postharvest Sweet Potato (Ipomoea Batatas (L.) Lam.)

Author

Bo Yuan, Xue-Wei Li, Ming-Jie Xu, Yu Zhang, Chun-Mei Zhang, Ke Xing, Cai Shurui, Sheng Qin, and Beibei Li

Subjects
Microbiology (medical), volatile organic compound, Ipomoea, Microbiology, fumigant, 03 medical and health sciences, Virology, Food science, Sugar, lcsh:QH301-705.5, Mycelium, 030304 developmental biology, 0303 health sciences, Rhizosphere, biology, 030306 microbiology, Chemistry, fungi, streptomyces lavendulae, biology.organism_classification, lcsh:Biology (General), Streptomyces lavendulae, Postharvest, Ceratocystis fimbriata, antimicrobial, ipomoea batatas (l.) lam, Black spot
Abstract

Black spot disease, which is caused by the pathogenic fungal Ceratocystis fimbriata, seriously affects the production of sweet potato and its quality during postharvest storage. In this study, the preliminary identification of the rhizosphere actinomycete strain SPS-33, and its antifungal activity of volatiles in vitro and in vivo was investigated. Based on morphological identification and phylogenetic analysis of the 16S rRNA gene sequence, strain SPS-33 was identified as Streptomyces lavendulae. Volatile organic compounds (VOCs) emitted by SPS-33 inhibited mycelial growth and sporulation of C. fimbriata in vitro and also induced a series of observable hyphae morphological changes. In an in vivo pathogenicity assay, exposure to SPS-33 significantly decreased the lesion diameter and water loss rate in sweet potato tuberous roots (TRs) inoculated with C. fimbriata. It increased the antioxidant enzymes’ activities of peroxidase, catalase, and superoxide dismutase as well as decreased malondialdehyde and increased total soluble sugar. In the VOC profile of SPS-33 detected by a headspace solid-phase micro extraction (HS-SPME) and gas chromatography-mass spectrometry (GC-MS), heptadecane, tetradecane, and 3-methyl-1-butanol were the most abundant compounds. 2-Methyl-1-butanol, 3-methyl-1-butanol, pyridine, and phenylethyl alcohol showed strong antifungal effects against C. fimbriata. These findings suggest that VOCs from S. lavendulae SPS-33 have the potential for pathogen C. fimbriata control in sweet potato postharvest storage by fumigant action.

Published
2020

22. A Novel Estrogen Receptor β Agonist Diminishes Ovarian Cancer Stem Cells via Suppressing the Epithelial-to-Mesenchymal Transition.

Author

Banerjee, Ananya, Cai, Shurui, Xie, Guozhen, Li, Na, Bai, Xuetao, Lavudi, Kousalya, Wang, Kevin, Zhang, Xiaoli, Zhang, Junran, Patnaik, Srinivas, Backes, Floor J., Bennett, Chad, and Wang, Qi-En

Subjects
*THERAPEUTIC use of antineoplastic agents, *DISEASE progression, *OVARIAN epithelial cancer, *ANTINEOPLASTIC agents, *METASTASIS, *CANCER relapse, *ESTROGEN receptors, *EPITHELIAL-mesenchymal transition, *GENE expression, *STEM cells, *CELL lines, *PHARMACODYNAMICS
Abstract

Simple Summary: Estrogen receptors α (ERα) and β (ERβ) show distinct contributions to tumor initiation and progression. Given that ERβ mainly functions as a "tumor suppressor", activation of ERβ using its specific agonist should be able to inhibit tumor progression. In this study, we show that a newly developed ERβ agonist, OSU-ERb-12, can not only impede ovarian cancer cell expansion and tumor growth but also reduce the cancer stem cell (CSC) population. OSU-ERb-12 could inhibit epithelial-to-mesenchymal transition (EMT) in ovarian cancer cells by increasing Snail expression, thereby, blocking EMT-mediated cancer cell dedifferentiation. We also found that OSU-ERb-12 inhibits ovarian cancer expansion in an ERα-independent manner while limiting the CSC population in an ERα-dependent manner. Taken together, our data suggest that the newly developed ERβ agonist OSU-ERb-12 can be used not only to hinder tumor growth but also has the potential to prevent tumor relapse and metastasis by depleting CSCs. Epithelial ovarian cancer is the most lethal malignancy of the female reproductive tract. A healthy ovary expresses both Estrogen Receptor α (ERα) and β (ERβ). Given that ERα is generally considered to promote cell survival and proliferation, thereby, enhancing tumor growth, while ERβ shows a protective effect against the development and progression of tumors, the activation of ERβ by its agonists could be therapeutically beneficial for ovarian cancer. Here, we demonstrate that the activation of ERβ using a newly developed ERβ agonist, OSU-ERb-12, can impede ovarian cancer cell expansion and tumor growth in an ERα-independent manner. More interestingly, we found that OSU-ERb-12 also reduces the cancer stem cell (CSC) population in ovarian cancer by compromising non-CSC-to-CSC conversion. Mechanistically, we revealed that OSU-ERb-12 decreased the expression of Snail, a master regulator of the epithelial-to-mesenchymal transition (EMT), which is associated with de novo CSC generation. Given that ERα can mediate EMT and facilitate maintenance of the CSC subpopulation and that OSU-ERb-12 can block the transactivity of ERα, we conclude that OSU-ERb-12 reduces the CSC subpopulation by inhibiting EMT in an ERα-dependent manner. Taken together, our data indicate that the ERβ agonist OSU-ERb-12 could be used to hinder tumor progression and limit the CSC subpopulation with the potential to prevent tumor relapse and metastasis in patients with ovarian cancer. [ABSTRACT FROM AUTHOR]

Published
2022
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24. ALDH1A1 Contributes to PARP Inhibitor Resistance via Enhancing DNA Repair in BRCA2−/− Ovarian Cancer Cells

Author

Liu, Lu, primary, Cai, Shurui, additional, Han, Chunhua, additional, Banerjee, Ananya, additional, Wu, Dayong, additional, Cui, Tiantian, additional, Xie, Guozhen, additional, Zhang, Junran, additional, Zhang, Xiaoli, additional, McLaughlin, Eric, additional, Yin, Ming, additional, Backes, Floor J., additional, Chakravarti, Arnab, additional, Zheng, Yanfang, additional, and Wang, Qi-En, additional

Published
2020
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26. Abstract GMM-017: UPREGULATION OF MIR-328 CONTRIBUTES TO OVARIAN CANCER STEM CELL MAINTENANCE BY DOWNREGULATING DDB2

Author

Srivastava, Amit Kumar, primary, Cui, Tiantian, additional, Banerjee, Ananya, additional, Han, Chunhua, additional, Cai, Shurui, additional, Liu, Lu, additional, Wu, Dayong, additional, Cui, Ri, additional, Li, Zaibo, additional, Zhang, Xiaoli, additional, Xie, Guozhen, additional, Karuppalyah, Selvendiran, additional, Karpf, Adam, additional, Liu, Jinsong, additional, Cohn, David, additional, and Wang, Qi-En, additional

Published
2019
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28. Inhibition of miR-328–3p Impairs Cancer Stem Cell Function and Prevents Metastasis in Ovarian Cancer

Author

Srivastava, Amit K., primary, Banerjee, Ananya, additional, Cui, Tiantian, additional, Han, Chunhua, additional, Cai, Shurui, additional, Liu, Lu, additional, Wu, Dayong, additional, Cui, Ri, additional, Li, Zaibo, additional, Zhang, Xiaoli, additional, Xie, Guozhen, additional, Selvendiran, Karuppaiyah, additional, Patnaik, Srinivas, additional, Karpf, Adam R., additional, Liu, Jinsong, additional, Cohn, David E., additional, and Wang, Qi-En, additional

Published
2019
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31. ERK Inactivation Enhances Stemness of NSCLC Cells via Promoting Slug-mediated Epithelial-to-mesenchymal Transition

Author

Cai, Shurui

Subjects
Biomedical Research, Biology, Genetics
Abstract

Lung cancer is the leading cause of cancer-related mortality globally, and non-small-cell lung cancer (NSCLC) represents the major histological subtype of lung cancer. Despite improved treatment methods within the past decades, NSCLC still has an inferior prognosis, and the 5-year survival rate remains as low as only 20%. The Mitogen-activated protein kinase (MAPK) pathway through the RAS-RAF-MEK-ERK signaling cascades is an evolutionarily conserved, intracellular signal transduction pathway that regulates various cellular processes including proliferation, differentiation, stress response, survival, and apoptosis. Importantly, dysregulated MAPK signaling is implicated in a wide range of cancers including NSCLC. Aside from regular chemo- and radio- cancer therapies, multiple kinase-inhibitors targeting the MAPK pathway have been developed. Currently, BRAF and MEK combination treatment is a standard care for treating BRAF V600E mutant NSCLC patients. Although the initial response to combination treatment was promising, the majority of the patients would develop tumor relapse and disease progression within one year. Multiple resistance mechanisms have been identified, and central to these mechanisms is the reactivation of the ERK signaling, which enables the rapid recovery of the MAPK signaling. In order to overcome the drug resistance and tumor relapse after BRAF and MEK inhibitors treatment, several ERK inhibitors have been developed and are in various stages of clinical trials. However, tumor relapse and disease progression are still observed after ERK inhibition. Tumors are highly heterogeneous, with subsets of cells showing distinct morphological and molecular profiles. Cancer stem cells (CSCs) are subpopulations of cancer cells identified in tumors that possess stem cell features. Similar to embryonic stem cells (ESCs), CSCs are characterized by the capacity for self-renewal and the ability to differentiate into diverse cancer cells. Substantial studies have shown that cancer stem cells exhibit extremely high tumorigenicity; Therefore, CSCs are also known as tumor-initiating cells. Importantly, CSCs are also responsible for multidrug resistance, contributing to tumor relapse and metastasis.The epithelial-to-mesenchymal transition (EMT) is a highly dynamic process by which epithelial cells lose their apical-basal polarity and cell-cell adhesion, and convert into a mesenchymal phenotype with migratory and invasive properties. EMT has been found to play a central role in normal physiological events such as embryonic development, tissue repair, and wound healing. EMT has also been implicated in pathological events such as carcinoma invasion and cancer metastasis in recent years. Furthermore, studies indicated that metastatic cancer cells, presumably undergoing EMT, could acquire CSC features.To best study the underlying mechanism of tumor relapse after ERK inhibitor treatment, we treated various NSCLC cell lines and a NSCLC patient-derived xenograft (PDX) harboring aberrant MAPK signaling with two selective ERK inhibitors, respectively Ulixertinib (BVD-523) and SCH772984, and found that ERK inhibition expanded the CSC population. To understand the mechanism of CSC enrichment after ERK inhibitor treatment, we performed an RNA-Seq analysis on BVD-523-treated A549 cells. Gene Set Enrichment Analysis (GSEA) showed an enriched EMT program in BVD-523-treated cells. We next validated the activated EMT program in NSCLC cell lines after ERK inhibitor treatment at RNA and protein levels, as well as their ability of migration and invasion. Since EMT is mainly triggered by the core EMT transcription factors (EMT-TFs), we analyzed the expression of these EMT-TFs in NSCLC cell lines. RNA-Seq data and further qRT-PCR validation revealed Snai2 (encodes for Slug protein) was the most induced EMT-TFs after ERK inhibitor treatment. To further characterize Slug as an EMT inducer in NSCLC cells treated with ERK inhibitor, we knocked down Slug using siRNA, and found ERK inhibitor was unable to induce EMT in NSCLC cells. Mechanistically, we revealed that ERK inhibition upregulates Slug by activating the JAK/STAT pathway. Specifically, we found that ERK inhibition increased phosphorylation of STAT3 at Y705 in NSCLC cell lines. Finally, we showed that the JAK/STAT pathway inhibitor Ruxolitinib could block the ERK inhibitor-induced EMT and CSC expansion, providing a feasible combination inhibitor approach for treating NSCLC patients harboring aberrant MAPK signaling. Taken together, this study revealed an unintended consequence of ERK inhibition in the treatment of MAPK pathway-driven NSCLC, ascertained the underlying mechanisms, and provided a promising strategy to prevent tumor relapse in patients.

Published
2022

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