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Previous studies have shown that calycosin, a natural phytoestrogen which is structurally similar to estrogen, inhibits proliferation and induces apoptosis in estrogen‑dependent cancer types via the estrogen receptor (ER)β‑induced inhibition of PI3K/Akt. Therefore, the aims of the present study were to investigate the effects of calycosin on human osteosarcoma (OS), and to examine the molecular mechanisms associated with ERβ. Human OS MG‑63&nbsp;cells were treated with various concentrations of calycosin, and MTT and flow cytometry assays were used to assess the effects of calycosin on cellular proliferation and apoptosis. In addition, protein expression levels of ERβ, phosphorylated (p)‑PI3K, p‑Akt, cleaved poly (ADP‑ribose) polymerase&nbsp;1 (PARP) and cleaved caspase‑3 were evaluated by western blot analysis. The present results suggested that calycosin inhibited proliferation and induced apoptosis in MG‑63&nbsp;cells. Furthermore, increased ERβ expression was detected in OS MG‑63&nbsp;cells treated with calycosin, and an ERβ inhibitor (PHTPP) reversed calycosin‑induced cytotoxicity and apoptosis. Moreover, phosphorylation levels of PI3K and Akt were significantly downregulated after calycosin treatment, whereas PHTPP reversed their phosphorylation. ERβ‑mediated PI3K/Akt downstream signaling pathways were found to influence the activity of poly (ADP‑ribose) polymerase&nbsp;1 and caspase‑3. Thus, the present results indicated that calycosin inhibited proliferation and induced apoptosis in OS MG‑63&nbsp;cells, and that these effects were mediated by ERβ‑dependent inhibition of the PI3K/Akt pathways.Lung cancer is the most prevalent cancer worldwide and non‑small cell lung cancer (NSCLC) is the most common subtype and accounts for 75% of all lung cancer cases. Although programmed death‑1/programmed death‑ligand‑1 (PD‑1/PD‑L1) blockade has shown good results in the clinic, numerous NSCLC patients still fail to respond to this therapy. In the current study, formalin‑fixed, paraffin‑embedded tumor and matched blood samples from 1,984 Chinese NSCLS patients were collected for detection of genomic alterations including single nucleotide variations, short and long insertions/deletions, copy number variations and gene rearrangements. The most common mutated genes were tumor protein p53 (55.70%; 1,105/1,984), epidermal growth factor receptor (52.47%; 1,041/1,184), KRAS proto‑oncogene GTPase (13.36%, 265/1084), cyclin dependent kinase inhibitor&nbsp;2A (12.30%; 244/1,984), LDL receptor related protein&nbsp;1B (11.09%; 220/1,984) and telomerase reverse transcriptase (10.58%; 210/1,984). Tumor mutational burden was calculated and results revealed that it was associated with PI3K/mTOR pathway gene mutations, and patient's gender, age, smoking status, and tumor stage. In addition, mutations of phosphatidylinositol‑4,5‑bisphosphate 3‑kinase catalytic subunit α or F‑box and WD repeat domain containing 7 were detected in 3 patients with NSCLC who were resistant to PD‑1 inhibitors nivolumab and pembrolizumab. Disease stabilization and tumor shrinkage were observed in these patients after mTOR inhibitor everolimus treatment. The current data showed that NSCLC with PI3K/mTOR mutations are sensitive to mTOR inhibitors.Protease inhibitors (PIs) inhibit HIV‑1 and HIV‑2 proteases, impeding virus replication and liberation of viral elements from infected cells. In human immunodeficiency virus&nbsp;(HIV) subjects receiving PI‑based treatment, an impressive decrease in the amount of HIV‑associated cancers, unconnected to viral burden or CD4 amount was observed. Research has reported that PIs have influence on cancer proliferation, spread, and survival as an effect on endoplasmic reticulum stress, proteasome, NF‑κB and Akt signalling. Nelfinavir&nbsp;(NFV) is a nonpeptidic PI that functions by connecting to the catalytic site of the HIV protease, thus stopping the cleavage of viral polyprotein into complete, operative proteins that are fundamental for viral survival. NFV, currently not frequently employed for antiretroviral treatment, has demonstrated noteworthy off target effects in tumor patients with or without HIV disease. NFV appears to cause cell death in tumor cells by different mechanisms, which include necrosis, apoptosis and autophagy. In this review, data from preclinical research and clinical trials are reported and the mechanisms of action of NFV and their results in the treatment of hematologic malignancies, such as acute myeloid leukemia, chronic lymphoid leukemia, and diffuse large B&nbsp;cell lymphoma, and especially in patients with multiple myeloma are examined. In the future, experimental studies may help identify the role of NFV in cancer treatment and may promote the application of this drug into daily clinical practice.Abnormal protein acetylation and succinylation in lysine residues can cause the initiation and development of numerous different types of tumors. However, to the best of our knowledge, there is currently a lack of systematic investigation in breast cancer. Using proteomic techniques, the present study systematically investigated the two modifications of all proteins in invasive ductal carcinoma tissues to identify potential targets. The results revealed significantly higher modification levels for the majority of proteins in breast cancer tissue when compared with para‑carcinomous normal tissue. The bioinformatic analysis demonstrated that either highly acetylated or succinylated proteins were significantly enriched in histone H2A.X (H2A.X) complexes and nucleophosmin (NPM1) may be the key member among them. The results of further analyses revealed that H2A.X complexes were associated with DNA damage response (DDR), and the proteomic results for protein quantification provided further evidence for the abnormal DDR condition in breast cancer tissues. Later, the western blotting results validated the high acetylation and succinylation levels of the majority of proteins, including the modification of NPM1 and its correlation with cell viability. Finally, the upregulation of H2A.X in breast cancer tissues further demonstrated the association between H2A.X complex modification and DDR in breast cancer. [https://www.selleckchem.com/products/paquinimod.html paquinimod] Overall, the present study systematically investigated the protein acetylation and succinylation in breast cancer and provided evidence to support H2A.X complexes as potential targets. These results broaden the horizon for breast cancer investigation and link it with epigenetics.