Tumor-derived lactate promotes resistance to bevacizumab treatment by facilitating autophagy enhancer protein RUBCNL expression through histone H3 lysine 18 lactylation (H3K18la) in colorectal cancer.

MLA

Li, Weihao, et al. “Tumor-Derived Lactate Promotes Resistance to Bevacizumab Treatment by Facilitating Autophagy Enhancer Protein RUBCNL Expression through Histone H3 Lysine 18 Lactylation (H3K18la) in Colorectal Cancer.” Autophagy, vol. 20, no. 1, Jan. 2024, pp. 114–30. EBSCOhost, https://doi.org/10.1080/15548627.2023.2249762.

APA

Li, W., Zhou, C., Yu, L., Hou, Z., Liu, H., Kong, L., Xu, Y., He, J., Lan, J., Ou, Q., Fang, Y., Lu, Z., Wu, X., Pan, Z., Peng, J., & Lin, J. (2024). Tumor-derived lactate promotes resistance to bevacizumab treatment by facilitating autophagy enhancer protein RUBCNL expression through histone H3 lysine 18 lactylation (H3K18la) in colorectal cancer. Autophagy, 20(1), 114–130. https://doi.org/10.1080/15548627.2023.2249762

Chicago

Li, Weihao, Chi Zhou, Long Yu, Zhenlin Hou, Huashan Liu, Lingheng Kong, Yanbo Xu, et al. 2024. “Tumor-Derived Lactate Promotes Resistance to Bevacizumab Treatment by Facilitating Autophagy Enhancer Protein RUBCNL Expression through Histone H3 Lysine 18 Lactylation (H3K18la) in Colorectal Cancer.” Autophagy 20 (1): 114–30. doi:10.1080/15548627.2023.2249762.