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16 results on '"Zeng, Zekun"'

12. Additional file 2 of ZIP10 is a negative determinant for anti-tumor effect of mannose in thyroid cancer by activating phosphate mannose isomerase

Author

Ma, Sharui, Wang, Na, Liu, Rui, Zhang, Rui, Dang, Hui, Wang, Yubo, Wang, Simeng, Zeng, Zekun, Ji, Meiju, and Hou, Peng

Abstract

Additional file 2: Figure S1. The effect of mannose on the proliferation of immortalized thyroid cell line Hthy-ori3���1. Figure S2. The effect of mannose on cell cycle distributions in thyroid cancer cells. Figure S3. The effect of PMI knockdown on cell cycle distributions in thyroid cancer cells. Figure S4. The effect of PMI knockdown on its enzyme activity. Figure S5. Zn2+ chelator TPEN increases the response of mannose-insensitive cell lines K1 and 8505C to mannose. Figure S6. Distinct expression of ZIP10 in thyroid cancer cell lines. Figure S7. Oncogenic role of ZIP10 in thyroid cancer cells. Figure S8. The effect of mannose on cell cycle distributions in ZIP10 knockdown-thyroid cancer cells. Figure S9. In vivo anti-tumor effect of mannose.

Published
2021
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13. Additional file 1 of ZIP10 is a negative determinant for anti-tumor effect of mannose in thyroid cancer by activating phosphate mannose isomerase

Author

Ma, Sharui, Wang, Na, Liu, Rui, Zhang, Rui, Dang, Hui, Wang, Yubo, Wang, Simeng, Zeng, Zekun, Ji, Meiju, and Hou, Peng

Abstract

Additional file 1: Table S1. The STR DNA profiling of cell lines used in this study. Table S2. Short interfering RNAs (siRNAs) used in this study. Table S3. Lentivirus short hairpin RNAs (sh-RNAs) used in this study. Table S4. The primer sequences used in this study.

Published
2021
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14. Additional file 1 of Atovaquone-HSA nano-drugs enhance the efficacy of PD-1 blockade immunotherapy by alleviating hypoxic tumor microenvironment

Author

Wang, Simeng, Zhou, Xinrui, Zeng, Zekun, Sui, Mengjun, Chen, Lihong, Feng, Chao, Huang, Chen, Yang, Qi, Ji, Meiju, and Hou, Peng

Subjects
body regions
Abstract

Additional file 1: Figure S1. In vitro toxicity evaluation of atovaquone. Figure S2. The average blooddrug concentration-time curves of HSA-ATO NPs and atovaquone.

Published
2021
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15. A promoted PtFe/SiO2catalyst with low Pt concentration for propane dehydrogenationElectronic supplementary information (ESI) available. See DOI: https://doi.org/10.1039/d3cy00060e

Author

Luo, Lei, Zeng, Zekun, Zhou, Tao, Luo, Jun, Chen, Xiaoheng, Li, Xu, Yan, Han, and Zeng, Jie

Abstract

Non-oxidative propane dehydrogenation (PDH) has developed into one major way to increase propylene production because of its unique advantages. The harsh reaction conditions put forward higher requirements for the activity and stability of catalysts. Herein, we successfully prepared PtFe/SiO2that presents excellent catalytic performances for PDH. The introduction of an Fe component is conducive to the high dispersion of Pt and restrains the migration of Pt that leads to agglomeration. Electrons are transferred from Fe to Pt species, forming an electron-rich Pt state that facilitates propane adsorption and propylene desorption. Meanwhile, electron-rich Pt sites are created in PtFe/SiO2, leading to the improvement of both propylene formation rate and mean lifetime compared to Pt/SiO2. PtFe/SiO2exhibits good catalytic activity and high stability with nearly 100% propylene selectivity. The initial C3H6formation rate reached 39.52 molpropylenegPt−1h−1and the mean lifetime was 83 h under these conditions: 500 °C, C3H8/H2/Ar = 1/1/8 and a weight hourly space velocity (WHSV) for propane of 24 h−1. As the WHSV increased to 48 h−1, the initial C3H6formation rate could reach 72.75 molpropylenegPt−1h−1. This work paves the way for developing robust Pt-based PDH catalysts viaalloying with earth-abundant metals.

Published
2023
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16. Targeting METTL3 enhances the chemosensitivity of non-small cell lung cancer cells by decreasing ABCC2 expression in an m 6 A-YTHDF1-dependent manner.

Author

Zhang R, Chen P, Wang Y, Zeng Z, Yang H, Li M, Liu X, Yu W, and Hou P

Subjects
Humans, Cell Line, Tumor, Animals, Drug Resistance, Neoplasm genetics, Mice, Paclitaxel pharmacology, Paclitaxel therapeutic use, Mice, Nude, Carboplatin pharmacology, Carboplatin therapeutic use, Adenosine analogs & derivatives, Adenosine metabolism, Adenosine pharmacology, Carcinoma, Non-Small-Cell Lung metabolism, Carcinoma, Non-Small-Cell Lung drug therapy, Carcinoma, Non-Small-Cell Lung genetics, Multidrug Resistance-Associated Proteins metabolism, Multidrug Resistance-Associated Proteins genetics, RNA-Binding Proteins metabolism, RNA-Binding Proteins genetics, Methyltransferases metabolism, Methyltransferases genetics, Lung Neoplasms metabolism, Lung Neoplasms drug therapy, Lung Neoplasms genetics, Lung Neoplasms pathology, Multidrug Resistance-Associated Protein 2 metabolism
Abstract

Patients with non-small cell lung cancer (NSCLC) are easily resistant to first-line chemotherapy with paclitaxel (PTX) or carboplatin (CBP). N 6 -methyladenosine (m 6 A) methyltransferase-like 3 (METTL3) has crucial functions in m 6 A modification and tumorigenesis. However, its role in chemoresistance of NSCLC is still elusive. Here, we demonstrated that METTL3 inhibitor STM2457 significantly reduced the IC 50 values of PTX or CBP in NSCLC cells, and they showed a synergistic effect. Comparing with monotherapy, a combination of STM2457 and PTX or CBP exhibited more potent in vitro and in vivo anti-tumor efficacy. In addition, we found that ATP binding cassette subfamily C member 2 (ABCC2) was responsively elevated in cytomembrane after PTX or CBP treatment, and targeting METTL3 could reverse this effect. Mechanistically, targeting METTL3 decreased the m 6 A modification of ABCC2 mRNA and accelerated its mRNA degradation. Further studies revealed that YTHDF1 could bind and stabilize the m 6 A-modified mRNA of ABCC2 , while YTHDF1 knockdown promoted it mRNA degradation. These results, taken together, demonstrate that targeting METTL3 enhances the sensitivity of NSCLC cells to PTX or CBP by decreasing the cytomembrane-localized ABCC2 in an m 6 A-YTHDF1-dependent manner, and suggest that METTL3 may be a potential therapeutic target for acquired resistance to PTX or CBP in NSCLC., Competing Interests: Competing Interests: The authors have declared that no competing interest exists., (© The author(s).)

Published
2024
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