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N-trans-Feruloyloctopamine (FO), a natural compound, was reported in our previous study to inhibit a tumor cell malignant phenotype by AKT- and EMT-related signals and might be used as a promising drug for HCC treatment. However, the specific targets and detailed mechanisms still need to be clarified. Screening with RNA-Seq in Huh7 cells treated with FO revealed that 317 genes were modulated, of which 188 genes were upregulated and 129 genes were downregulated. Real-time cell analyzer and flow cytometry data reveal that tumor cell proliferation and apoptosis were impacted by FO. DAVID bioinformatic data showed that most of the biological process GO terms are related to proliferation and apoptosis. KEGG enrichment analysis showed that FO mainly regulates PI3K-AKT- and apoptosis-related signals, in which BBC3, DDIT3, NOXA, and CDKN1A on the surface serve as the novel targets of FO inducing HCC cell apoptosis. The result implied that FO might exacerbate HCC cell apoptosis by regulating BBC3, DDIT3, CDKN1A, and NOXA signals. The obstacle effect of FO can provide new targets and new credibility for the treatment of liver cancer.

N-trans-Feruloyloctopamine (FO), a natural compound, was reported in our previous study to inhibit a tumor cell malignant phenotype by AKT- and EMT-related signals and might be used as a promising drug for HCC treatment. However, the specific targets and detailed mechanisms still need to be clarified. Screening with RNA-Seq in Huh7 cells treated with FO revealed that 317 genes were modulated, of which 188 genes were upregulated and 129 genes were downregulated. Real-time cell analyzer and flow cytometry data reveal that tumor cell proliferation and apoptosis were impacted by FO. DAVID bioinformatic data showed that most of the biological process GO terms are related to proliferation and apoptosis. KEGG enrichment analysis showed that FO mainly regulates PI3K-AKT- and apoptosis-related signals, in which BBC3, DDIT3, NOXA, and CDKN1A on the surface serve as the novel targets of FO inducing HCC cell apoptosis. The result implied that FO might exacerbate HCC cell apoptosis by regulating BBC3, DDIT3, CDKN1A, and NOXA signals. The obstacle effect of FO can provide new targets and new credibility for the treatment of liver cancer.

Carcinogenesis is known to be primarily associated with gene mutations. Recently, increasing evidence has suggested that epigenetic events also serve crucial roles in tumor etiology. Environmental factors, including nutrition, toxicants and ethanol, are involved in carcinogenesis through inducing epigenetic modifications, such as DNA methylation, histone deacetylase and miRNA regulation. Studying epigenetic mechanisms has facilitated the development of early diagnostic strategies and potential therapeutic avenues. Modulation at the epigenetic level, including reversing epigenetic modifications using targeted drugs, has demonstrated promise in cancer therapy. Therefore, identifying novel epigenetic biomarkers and therapeutic targets has potential for the future of cancer therapy. The present review discusses the environmental factors involved in epigenetic modifications and potential drug candidates for cancer therapy.

Cancer related fatigue significantly disrupts normal life for a portion of cancer survivors, and may persist for many years with cancer patients. Fatigue lasts longer than other treatment side-effects. There are increasing reports of using immunocyte therapy to treat cancer, and if it could be alternative relieve therapy in persons with cancer related fatigue is not so clear. Herein, we retrospectively evaluated the improvement of cancer related fatigue and safety of this therapy administered to cancer patients. 539 patients were treated with immunocyte therapy after conventional treatment. Methods: The delayed-type hyper-sensitivity (DTH) skin test was used to measure the immune response. Investigated into cancer related fatigue, physical strength, appetite and sleep as clinical efficacy. Results: The DTH skin tests showed that the positive cell-mediated cytotoxicity response rate was 82.7%. A large proportion of patients’ cancer related fatigue (80%); appetite (94.1%), sleeping status (96.6%) and metal state (92.9%) were improved. Adverse reactions were fever (35.1%), insomnia (21.4%), anorexia (15.7%), arthralgia (8%), rash (3.3%). DC (dendritic cell) therapy combined with CIK (cytokine-induced killer cell) was observed no toxicity in patients. Conclusion: This is the first time we reported combination of DC and CIK therapy to relieve the cancer related fatigue of patients after conventional therapy (surgery, radiotherapy, and chemotherapy). It may be an effective immunotherapy to reduce adverse reactions and a safety treatment. The data of CIK treatment time and CIK cell number provide strong support for further clinical treatment.