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Published in Valerio Voliani, Nanomaterials and Neoplasms, 2021
Eun-Kyung Lim, Taekhoon Kim, Soonmyung Paik, Seungjoo Haam, Yong-Min Huh, Kwangyeol Lee
As described earlier, cancer cells undergo a series of changes via mutation and eventually acquire a number of abilities, dubbed as hallmarks for cancer [29, 30], such as self-sufficiency in growth signals, insensitivity to antigrowth signals, evasion of apoptosis, limitless replication, sustained angiogenesis, tissue invasion and metastasis, deregulation of cellular energetics, and escape from immune destruction, which distinguishes cancer cells from normal cells. The detailed discussion of these hallmarks does not need to be repeated here, but it should be stressed that a thorough understanding of cancer metabolism is imperative for successful design of nanomaterial-based theranostic agents.
The Advantages and Versatility of Carrier-Free Nanodrug and Nanoparticle Systems for Cancer Therapy
Published in Loutfy H. Madkour, Nanoparticle-Based Drug Delivery in Cancer Treatment, 2022
Malignant cells are resistant to the anticancer action [170] of chemotherapeutic agents and cell division inhibitors, which reflects their ability to change at molecular level and develop tumor survival strategies that activate the angiogenic mechanism, in order to prevent hypoxic conditions and to support nutrient intake. Therefore, the main therapeutic approaches are targeting the hallmarks of cancer, particularly aiming to inhibit tumor angiogenesis. Multiple cellular processes related to apoptosis or cell proliferation lead to alterations in signaling pathways that are responsible for resistance to chemotherapy and drug tolerance in a cancer cell [171–173].
The Role of Nanotechnology in the Treatment of Drug Resistance Cancer
Published in Bhaskar Mazumder, Subhabrata Ray, Paulami Pal, Yashwant Pathak, Nanotechnology, 2019
Sandipan Dasgupta, Anup Kumar Das, Paulami Pal, Subhabrata Ray, Bhaskar Mazumder
After a sufficient amount of anticancer drug has entered, accumulated, and inhibited its cellular targets, the outcome is dependent on how the cancer cell reacts. Ideally, anticancer drug-induced damage results in cancer cell death. However, several intrinsic adaptive responses are triggered that promote cancer cell survival. Additionally, the pathways that regulate cell death through apoptosis frequently become dysfunctional, which has become one of the hallmarks of cancer (Hanahan and Weinberg, 2000).
MicroRNA-122 overexpression promotes apoptosis and tumor suppressor gene expression induced by microcystin-leucine arginine in mouse liver
Published in International Journal of Environmental Health Research, 2022
Rui Wang, Haohao Liu, Xingde Du, Ya Ma, Zhihui Tian, Shiyu Zhang, Linjia Shi, Hongxiang Guo, Huizhen Zhang
The induction of apoptosis caused by DNA damage in precancerous lesions can remove potentially harmful cells, thereby blocking tumor growth. Deregulation of this death process is associated with unchecked cell proliferation, development and progression of cancer and cancer resistance to drug therapies Fulda (2009). For these reasons, deregulation of apoptosis is considered one of the hallmarks of cancer. It had been reported that miR-122 could serve as a pro-apoptotic factor in suppressing hepatocellular carcinoma cell migration and invasion Wang et al. (2018). Studies have shown that miR-122 can participate in apoptosis of liver cancer cells by regulating many pathways such as the programmed cell death 4 (PDCD4) signaling pathway Wang et al. (2018).