Glutamine metabolism in breast cancer and possible therapeutic targets.

Exosomal circRNAs in cancer: Implications for therapy resistance and biomarkers.

Cancer is a multi-factor systemic malignant disease, which has seriously threatened human health and created a heavy burden on the world economy. Metabolic reprogramming, one of the important signs of malignant tumours, provides necessary nutrition for tumorigenesis and cancer development; thus, it has recently become a research hot spot, even though the metabolic mechanism is quite intricate. Circular RNA (circRNA) affects cancer cell metabolism through various molecular mechanisms, playing an important role in promoting or suppressing cancer. Because of the structure characteristics, circRNA is quite stable, and can be utilized as biomarkers. In this review, we analysed and summarized the characteristics and biological functions of circRNA and comprehensively reviewed and discussed the important role of circRNA in cancer metabolic reprogramming. This review will provide new ideas for developing new anti-cancer therapeutic targets, mining cancer diagnostic and prognostic markers, and will provide guidance for other researchers to design circRNA-related experiments and develop anti-tumour drugs. 

Research progress of circRNA in malignant tumour metabolic reprogramming

Prostate carcinoma is a malignant situation that arises from genomic alterations in the prostate, leading to changes in tumorigenesis. The NF-κB pathway modulates various biological mechanisms, including inflammation and immune responses. Dysregulation of NF-κB promotes carcinogenesis, including increased proliferation, invasion, and therapy resistance. As an incurable disease globally, prostate cancer is a significant health concern, and research into genetic mutations and NF-κB function has the efficacy to facilitate the introduction of novel therapies. NF-κB upregulation is observed during prostate cancer progression, resulting in increased cell cycle progression and proliferation rates. Additionally, NF-κB endorses resistance to cell death and enhances the capacity for metastasis, particularly bone metastasis. Overexpression of NF-κB triggers chemoresistance and radio-resistance, and inhibition of NF-κB by anti-tumor compounds can reduce cancer progression. Interestingly, non-coding RNA transcripts can regulate NF-κB level and its nuclear transfer, offering a potential avenue for modulating prostate cancer progression. 

Malignant function of nuclear factor-kappaB axis in prostate cancer: Molecular interactions and regulation by non-coding RNAs.

Abstract Breast cancer is one of the most common malignancies that pose a serious threat to women's health. Reprogramming of energy metabolism is a major feature of the malignant transformation of breast cancer. Compared to normal cells, tumor cells reprogram metabolic processes more efficiently, converting nutrient supplies into glucose, amino acid and lipid required for malignant proliferation and progression. Non-coding RNAs(ncRNAs) are a class of functional RNA molecules that are not translated into proteins but regulate the expression of target genes. NcRNAs have been demonstrated to be involved in various aspects of energy metabolism, including glycolysis, glutaminolysis, and fatty acid synthesis. This review focuses on the metabolic regulatory mechanisms and clinical applications of metabolism-regulating ncRNAs involved in breast cancer. We summarize the vital roles played by metabolism-regulating ncRNAs for endocrine therapy, targeted therapy, chemotherapy, immunotherapy, and radiotherapy resistance in breast cancer, as well as their potential as therapeutic targets and biomarkers. Difficulties and perspectives of current targeted metabolism and non-coding RNA therapeutic strategies are discussed. 

Metabolism-regulating non-coding RNAs in breast cancer: roles, mechanisms and clinical applications

Circ_0062558 promotes growth, migration, and glutamine metabolism in triple-negative breast cancer by targeting the miR-876-3p/SLC1A5 axis

Exosomes, which are small extracellular vesicles, have been unveiled to carry circular RNAs (circRNAs). CircRNA paired-related homeobox 1 (circPRRX1) can be transferred by exosomes derived from gastric cancer cells. Here, we investigated the activity and mechanism of exosomal circPRRX1 in gastric tumorigenesis and radiation sensitivity. CircPRRX1, microRNA (miR)-596, and NF-κB activating protein (NKAP) were quantified by quantitative real-time PCR and immunoblotting. Cell proliferation, motility, and invasion were detected by 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide and transwell assays, respectively. Cell colony formation and survival were assessed by colony formation assays. Dual-luciferase reporter assays were performed to verify the direct relationship between miR-596 and circPRRX1 or NKAP. In-vivo xenograft studies were used to evaluate the role of exosomal circPRRX1 in tumor growth. Our data showed that circPRRX1 expression was elevated in human gastric cancer, and circPRRX1 could be transferred by exosomes from gastric cancer cells. Exosomal circPRRX1 affected cell proliferation, motility, invasion, and radiation sensitivity in vitro and tumor growth in vivo. Mechanistically, circPRRX1 directly regulated miR-596 expression, and exosomal circPRRX1 affected cell biological functions at least in part through miR-596. NKAP was identified as a direct target and functionally downstream effector of miR-596. Exosomal circPRRX1 modulated NKAP expression by acting as a competing endogenous RNA (ceRNA) for miR-596. Our findings suggest a new mechanism, the exosomal circPRRX1/miR-596/NKAP ceRNA crosstalk, in regulating gastric tumorigenesis and radiation sensitivity.

Exosomal circPRRX1 functions as a ceRNA for miR-596 to promote the proliferation, migration, invasion, and reduce radiation sensitivity of gastric cancer cells via the upregulation of NF-κB activating protein

Lung cancer, a most common clinically diagnosed malignancy grows rapidly and undergoes metastasis/diffusion to distant organs at a fast rate. In the present study gravacridondiol tetrazole (tetrazole) was synthesized and investigated for lung cancer growth inhibition potential in vitro. MTT assay and flow cytometry using propidium iodide were used to determine viability changes and DNA content distribution. Protein expression and apoptotic changes were detected by western blotting and Annexin-V/PI assays. Treatment with 12 μM tetrazole suppressed viabilities to 23% and 20% in A549 and NCI-H1819 cells, respectively. In tetrazole exposed cells, G1-phase cell count increased significantly compared to the control. Tetrazole-treatment of A549 and NCI-H1819 cells caused a prominent raise in LC3‑II and p-ERK1/2 expression at 72 h. The SQSTM1/p62 level, p-mTOR and p-p70S6K expression was lowered significantly in A549 and NCI-H1819 cells on exposure to tetrazole. Exposure to U1026 alleviated tetrazole mediated LC3II/I ratio increase in A549 and NCI-H1819 cells significantly (P<0.02) compared to tetrazole treated cells. Treatment with tetrazole and 3‑MA in combination led a significant (P<0.02) elevation in A549 and NCI-H1819 cell apoptotic count relative to tetrazole (12 μM) alone treated cells. Moreover, tetrazole and 3‑MA combination increased cleavage of caspase‑3 to a greater extent compared to tetrazole. In summary, tetrazole manifested anti-proliferative effect on lung cancer cells via autophagy over-activation and arrest of cell cycle. It deactivated ERK1/2 signalling and promoted mTOR signaling in A549 and NCI-H1819 cells to regulate cancer proliferation. Thus, tetrazole needs to be studied further as an anti-proliferative agent for treatment of lung cancer.

/pdf/lung-cancer-growth-inhibition-and-autophagy-activation-by-2hwzcwyz.pdf

Lung cancer growth inhibition and autophagy activation by tetrazole via ERK1/2 up-regulation and mTOR/p70S6K signaling down-regulation.

: of on the of To investigate the effect of shikonin on the oxidative damage of lung cancer cells and promotes cell senescence through p53/p21Waf signaling pathway. The lung adenocarcinoma A549 cells were cultured and made into cell suspension. The lung adenocarcinoma A549 cells were cultured for 12 h, 24 h and 48 h respectively with different concentrations of shikonin (0 μm, 2 μm and 4 μm) and the activity of lung adenocarcinoma A549 cells was detected by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide method. The cell cycle of each group was measured by flow cytometry after 48 h of action of shikonin. The aging of each group of cells was determined by beta-galactosidase staining after 48 h of action of shikonin. The reactive oxygen species content in each group was determined by flow cytometry 48 h after the action of shikonin. The expression levels of cyclin D1, demethylase KDM2B, deoxyribonucleic acid damage marker protein p-H2AX, p53 and p21WAF were measured by Western blot. With the increase of shikonin concentration, the cell activity and the expression levels of cyclin D1 and KDM2B were significantly decreased, the proportion of resting phase/intermediate phase cells and senescent cells were significantly increased, the level of reactive oxygen species and the expression levels of p-H2AX, p53 and p21WAF were significantly increased (p<0.05). Shikonin can inhibit cell activity, induce oxidative damage and promote cell senescence, which may be achieved by activating p53/p21WAF signaling pathway.

/pdf/shikonin-induces-oxidative-damage-and-promotes-cell-3hx5xk4l.pdf

Shikonin Induces Oxidative Damage and Promotes Cell Senescence in Lung Cancer Cells through p53/p21WAF Signaling Pathway

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Circ_0062558 promotes growth, migration, and glutamine metabolism in triple-negative breast cancer by targeting the miR-876-3p/SLC1A5 axis

Exosomal circPRRX1 functions as a ceRNA for miR-596 to promote the proliferation, migration, invasion, and reduce radiation sensitivity of gastric cancer cells via the upregulation of NF-κB activating protein

Lung cancer growth inhibition and autophagy activation by tetrazole via ERK1/2 up-regulation and mTOR/p70S6K signaling down-regulation.

Shikonin Induces Oxidative Damage and Promotes Cell Senescence in Lung Cancer Cells through p53/p21WAF Signaling Pathway