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Introduction to Cancer, Conventional Therapies, and Bionano-Based Advanced Anticancer Strategies
Published in D. Sakthi Kumar, Aswathy Ravindran Girija, Bionanotechnology in Cancer, 2023
Cellular stress that activates P53 induces apoptosis. During the cell cycle arrest, the weak and sustained activation can promote cell death known as senescence. Cellular senescence is pathophysiological condition by which the cells permanently lose their proliferative capacity. Senescence cell shows specific-morphological features, including flattening, nuclear enlargement, enriched with vacuoles, and altered chromatin structure. In the biochemical level, cellular senescence is characterized by increased ß-galactocidase activity that increases senescence markers, such as P15, P16, P21, P53, and ARF.
Plantago ovata (Isabgol) and Rauvolfia serpentina (Indian Snakeroot)
Published in Azamal Husen, Herbs, Shrubs, and Trees of Potential Medicinal Benefits, 2022
Ankur Anavkar, Nimisha Patel, Ahmad Ali, Hina Alim
Other than use of reserpine as hypertensive drug it also shows activity against cancer cells both in vitro and in vivo. Experimental studies have reported an increase in life span of mice suffering from leukemia when administered with reserpine. Many other studies have reported antitumoral activity of reserpine against a variety of mouse sarcomas. A study was conducted using reserpine on drug-resistant tumor cells. Cell analysis reported cell cycle arrest in G1 phase. The reserpine proved effective against tumor cells by increasing intracellular drug accumulation and inhibition of P-glycoprotein. Reserpine improves the activity of anticancer and alkylating drugs. On the other hand, molecular docking showed reserpine binds strongly to receptors when compared to other drugs (Abdelfatah and Efferth, 2015). Reserpine is also an inhibitor of carcinogenesis in the liver caused by FAA (N-2-fluorenylacetamide). Currently, there are very few reports of reserpine being used for liver cancer treatment (Liu et al., 2019). Reserpine also has side effects on the cardiovascular system in patients suffering with just cancer. Thus, reserpine could be beneficial to cancer patients suffering from hypertension but could affect others suffering only from cancer. Thus, further studies are required on antitumor activity of reserpine (Abdelfatah and Efferth, 2015).
Chemopreventive Agents
Published in David E. Thurston, Ilona Pysz, Chemistry and Pharmacology of Anticancer Drugs, 2021
Sanguinarine is documented to have antitumor activity, and in vitro cytotoxicity in tumor cell lines at concentrations below 10 µM have been reported. Preliminary in vitro and in vivo studies have demonstrated that sanguinarine causes apoptosis in human cancer cells. For example, it has been shown to induce cell-cycle arrest at different phases of the cell cycle in cancer cells, and to promote apoptosis. It has also been shown to sensitize breast cancer cells to TNF-related apoptosis. Low doses of sanguinarine have been shown to cause apoptosis in human epidermoid carcinoma cells with little effect on healthy human skin cells at a similar dose. In in vivo studies sanguinarine has been shown to promote antiangiogenic effects in mice at a dose of 5 mg/kg, leading to anti-invasive effects. Based on this, it has been suggested that co-administration of sanguinarine with other therapeutic agents may be useful in the management of prostate cancer.
Cetuximab-conjugated PLGA nanoparticles as a prospective targeting therapeutics for non-small cell lung cancer
Published in Journal of Drug Targeting, 2023
Leena Kumari, Iman Ehsan, Arunima Mondal, Ashique Al Hoque, Biswajit Mukherjee, Pritha Choudhury, Arunima Sengupta, Ramkrishna Sen, Prasanta Ghosh
The cell cycle regulatory pathway is crucial to the initiation and development of tumours. The strong binding of DTX causes the mitotic arrest of cancer cells to microtubules and promotes its stability. It is well established that DTX causes cell cycle arrest by chromosomal breakage and mitotic impairment, leading to normal G2/M phase arrest. A decrease in the percentage of cells in the S phase and an accumulation of cells in the G2/M phase was seen in A549 and NCI-H23 cells after treatment with DTX, DTX NP, and Cet-DTX NP. The cells were treated with DTX, DTX-NPs, and Cet-DTX-NPs before incubating for 24 h. The control cells of the A549 and NCI-H23 cell lines were primarily in the G1 phase, with 8% and 9% of them in the G2/M phase (Figure 4C and D). Cet-DTX NP treatment significantly arrested the G2/M phase (39.3% and 36.6% in A549 and NCI-H23 cells, respectively). The results suggest that after the treatment with Cet-DTX NP, the cells were inhibited in interphase (G2/M phase), which promotes the arrest of mitotic cell division. Chromosome damage might be the underlying cause of cell cycle arrest.
A novel anticancer chromeno-pyrimidine analogue inhibits epithelial-mesenchymal transition in lung adenocarcinoma cells
Published in Toxicology Mechanisms and Methods, 2021
Venkateswarareddy Nallajennugari, Sankar Pajaniradje, Srividya Subramanian, Suhail Ahmad Bhat, Parthasarathi D, Savitha Bhaskaran, Syed Ali Padusha M, Rukkumani Rajagopalan
Cell death cannot be validated by a single experiment thereby other hallmark features of apoptosis such as loss of mitochondrial membrane potential (Zhu et al. 2015), laddering pattern of DNA (Green and Reed 1998) were evaluated. It was found that CP4b treated A549 cells showed decreased mitochondrial membrane potential compared to untreated cells indicating intrinsic mode of apoptotic induction. Laddering pattern of DNA in treated A549 cells confirmed the apoptotic mode of cell death. Cell cycle arrest can induce apoptosis. There was accumulation of cells in the G1 phase of cell cycle in CP4b treated A549 cells compared to untreated cells. Inhibition of wound closure in the CP4b treated cells when compared to untreated cells in the wound healing assay indicated that the migratory potential was hindered in the A549 cells by the drug, indicating the antimetastatic potential of CP4b.
MiR-34a reverses radiation resistance on ECA-109 cells by inhibiting PI3K/AKT/mTOR signal pathway through downregulating the expression of SIRT1
Published in International Journal of Radiation Biology, 2021
Zhimin Ye, Tieming Xie, Fengqin Yan, Lei Wang, Jun Fang, Zhun Wang, Fujun Hu, Fangzheng Wang, Zhenfu Fu
The efficiency of radiotherapy is impacted by many factors, among which p53 is of great significance. P53 is a tumor suppressor gene, which can suppress the proliferation of tumor cells by inducing cell cycle arrest and apoptosis under the situation of DNA damage (Shibata-Kobayashi et al. 2013). However, in most types of human tumors, p53 mutant is a normalcy, including EC (Whibley et al. 2009). As an important anti-tumor molecular, the expression level of p53 protein was regulated by plenty of transcription factors, such as miR-34a (Xiao et al. 2014). MiR-34a is a non-coding RNA discovered recently, which is involved in the inhibition of oncogenesis, tumor metastasis, tumor invasion, and the prevention of radiotherapy resistance (Dorn 2013). The expression level of miR-34a in tumor cells is relatively low and miR-34a is combined with RNA-induced silencing complex (RISC) to regulate the function of p53 pathway, which mediates the regulation of cell circle arrest, DNA damage repair, apoptosis, and cell aging (Shi et al. 2016).