Glioma is a worldwide malignancy, which displays significantly active metastasis and angiogenesis. Interaction between long non-coding RNAs (lncRNAs) and microRNAs (miRNAs) has been shown to play crucial role in regulating tumor properties. However, the potential of lncRNA X-inactive specific transcript (XIST) to function as a miRNA regulator and its relevance in glioma tumorigenicity and angiogenesis have so far remained unclear. Expression analysis of lncRNA XIST in glioma cells revealed its significant up-regulation. Interestingly, silencing of XIST repressed both metastatic and pro-angiogenic ability in vitro as well as in vivo. Subsequent studies revealed that lncRNA XIST expression inversely correlated with miR-429 expression in glioma cells; miR-429 modulated XIST expression by directly targeting the XIST gene sequence. In addition, miR-429 inhibitor restored metastatic and pro-angiogenic ability of gliomas abolished by silencing XIST. Our data provide insight into the key roles of the lncRNA-miRNA functional network in gliomas, which can aid in developing new therapeutic strategies for gliomas through clinical trials.

It has been found that the development of some cancers can be attributed to obesity, which is associated with the excessive intake of lipids. Cancer cells undergo metabolic reprogramming, shifting from utilizing glucose to fatty acids (FAs) for energy. CD36, a lipid transporter, is highly expressed in certain kinds of cancer cells. High expressions of CD36 in tumor cells triggers FA uptake and lipid accumulation, promoting rapid tumor growth and initiating metastasis. Meanwhile, immune cells in the tumor microenvironment overexpress CD36 and undergo metabolic reprogramming. CD36-mediated FA uptake leads to lipid accumulation and has immunosuppressive effects. This paper reviews the types of FAs associated with cancer, high expressions of CD36 that promote cancer development and progression, effects of CD36 on different immune cells in the tumor microenvironment, and the current status of CD36 as a therapeutic target for the treatment of tumors with high CD36 expression.

Exosomes are lipid membrane bilayer-encapsulated vesicles secreted by cells into the extracellular space. They carry abundant inclusions (such as nucleic acids, proteins, and lipids) that play pivotal roles in intercellular communication. Tumor stem cells are capable of self-renewal and are crucial for survival, proliferation, drug resistance, metastasis, and recurrence of tumors. The miRNAs (microRNAs) in exosomes have various functions, such as participating in inflammatory response, cell migration, proliferation, apoptosis, autophagy, and epithelial-mesenchymal transition. Tumor stem cells secrete exosomes that act as important messengers involved in various tumor processes and several studies provide increasing evidence supporting the importance of these exosomes in tumor recurrence and metastasis. This review primarily focuses on the production and secretion of exosomes from tumors and tumor stem cells and their effects on cancer progression. Cancer stem cancer derived exosome play an important massager in the tumor microenvironment. It also emphasizes on the study of tumor stem cell exosomes in the light of cancer metastasis and recurrence aiming to provide valuable insights and novel perspectives, which could be beneficial for developing effective diagnostic and treatment strategies.

Spandidos Publications is a scientific publisher with a long-standing international reputation for excellent standards and high quality science publications

The species in Sanghuangporus are a group of edible mushrooms with a long history of oral use in East Asia as a health-improvement method. They should be classified under the genus Sanghuangporus rather than mistakenly in Phellinus or Inonotus. The major components in this genus consist of polysaccharides, polyphenols, triterpenoids, and flavonoids, all of which exist in the fruiting bodies and mycelia. For extraction, studies have shown methods using hot water, ethanol, DES solvent, and alkaline, followed by purification methods including traditional anion column, Sevag solution, macroporous resin, and magnetic polymers. Proven by modern medical technology, these components possess promising anti-inflammatory, antioxidative, antitumor, and immunoregulation effects; additionally, they have health-improving effects including pulmonary protection, hypoglycemic properties, sleep improvement, gout mitigation, antiaging, neuroprotection, and muscle-strengthening abilities. Several toxicity studies have revealed their safety and recommend a dose of 1 g/kg for mice. As a newly emerged concept, functional food can provide not only life-sustaining nutrients but also some health-improving effects. In conclusion, we substantiate Sanghuang as a functional food by comprehensively presenting information on extraction and purification methods, component medical and structural properties, and nontoxicity, hoping to benefit the development of Sanghuang species as a group of functional food.

Tumor hypoxia contributes to the development of resistance to chemotherapeutic drugs in several human cancer cell lines. Atovaquone, an anti‑malaria drug approved by the US Food and Drug Administration, has recently demonstrated anti‑cancer effects in vitro and in vivo in several cancer models. To assess the potential of atovaquone as an anti‑cancer agent under hypoxia in colorectal carcinoma, EpCAM⁺CD44⁺ colon cancer stem cells were isolated from HCT‑116 human colon cancer cells through magnetic‑activated cell sorting. The efficacy of atovaquone on cytotoxicity, tumorsphere formation, apoptosis, invasion and cell‑cycle progression under hypoxic conditions were evaluated. MTS assays indicated that atovaquone inhibited the proliferation of EpCAM⁺CD44⁺ HCT‑116 cells with a half‑maximal inhibitory concentration of 15 µM. Atovaquone inhibited tumorsphere formation and cell proliferation by causing cell‑cycle arrest in S‑phase, which induced apoptosis of EpCAM⁺CD44⁺ HCT‑116 cells, as detected by Annexin V‑FITC/PI double staining assays, and caused mitochondrial membrane potential depolarization, as determined by a JC‑1 staining assay. Reverse transcription‑quantitative PCR demonstrated increased expression of Bax and downregulation of Bcl‑2. Transwell invasion assays indicated that atovaquone inhibited the invasiveness of EpCAM⁺CD44⁺ HCT‑116 cells under hypoxia, which was associated with upregulation of MMP‑2 and ‑9 and increased expression of tissue inhibitor of MMPs (TIMP)‑1. Taken together, atovaquone reduced the tumorsphere formation and invasion ability of EpCAM⁺CD44⁺ HCT‑116 cells, at least in part by increasing the expression of TIMP‑1 and downregulating the expression of MMP‑2 and ‑9, as well as the cells' viability by inducing cell‑cycle arrest in S‑phase and induction of apoptosis via the Bcl‑2/Bax pathway under hypoxic conditions. Further studies are warranted to explore the mechanisms of action of atovaquone as a promising anticancer agent in the treatment of colorectal carcinoma.