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Nickel chloride has also anticancer properties, according to new studies. It was found that NiCl 2 decreased cell viability in both cell lines in a dose- and time-dependent manner. Nickel chloride exposure at IC50 doses has been shown to reduce HCC cells' ability to produce colonies and cause apoptosis of HCC cells, as well as increased Cleaved Caspase-3 protein levels. In addition, NiCl 2 delayed cell migration, reduced the size and viability of HCC tumor spheroids cultured in 3D cell cultures, and disrupted tumor cell structure, which was found to differ depending on E-cadherin expression levels. In addition, it was discovered that all anticancer biological responses induced by NiCl 2 occurred independent of the AKT signaling pathway. In conclusion, our findings showed that NiCl 2 induced anticancer biological responses in HCC cell lines, according to our findings.
Source link: https://europepmc.org/article/MED/36628412
Method We independently carried out PDT and chemotherapy with sorafenib or doxorubicin in Huh-7 and Hep3b cell lines by raising the sorafenib or doxorubicin concentrations and raising the total energy of 808 nm light. Result The viability of the Huh-7 and Hep3B cell lines faded rapidly as the concentration of sorafenib or doxorubicin decreased, as the total energy of 808 nm light increased. Compared to PDT or chemotherapy alone, the cell viability of the Huh-7 and Hep3b cell lines with combined PDT and chemotherapy was less than that with combined PDT or chemotherapy alone. Tumor size was markedly reduced in the HCC PDoX mouse model, with complete remission achieved as compared to the single chemotherapy or PDT groups. Conclusion The synergistic results of concurrent PDT and chemotherapy in the HCC cell line and PDOX model were confirmed with no apparent adverse effect.
Source link: https://europepmc.org/article/MED/36623346
Our aim We investigated the effects of fusidic acid on human cervical, thyroid, and breast carcinoma cell lines to see whether FA might be useful in cancer treatment. The cell lines remained stable in each cell type after FA treatment, showing that growth inhibition by FA was not related to the induction of apoptosis. Cell cycle arrest at a dose that reduced growth rate was halted, but cell types were variable in different cell types. Using cell cycle arrest in human cervical, thyroid, and breast carcinoma cell lines, FA treatment can hinder cell proliferation by inducing cell cycle arrest.
Source link: https://europepmc.org/article/MED/36575560
Oral squamous cell carcinoma is the most common and widespread form of head and neck cancer. Patients with advanced disease have a 5-year survival rate that is less than half due to drug resistance. We focused on paraoxonase-2 enzyme in order to find molecular targets for safe oral cancer therapy. In HSC-3 and HOC621 oral cancer cell lines, gene silencing was achieved, and cell proliferation, viability, apoptosis induction, and responses to cisplatin and 5-fluorouracil treatment were investigated. In cisplatin-resistant clones obtained from HOC621 cell lines, as well as in parental cells, Enzyme level and cell proliferation were also determined. Spectroscopic results revealed that under cisplatin therapy, metabolic damage exerted on lipids and proteins was more apparent in cells down-regulating paraoxonase-2 than controls. Compared to control HOC621 cells, enzyme expression, as well as cell proliferation were all significantly elevated in cisplatin-resistant cells.
Source link: https://europepmc.org/article/MED/36613780
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