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Stem cells are characterized by the capability of self-renewal and multi-differentiation. Normal stem cells, which are important for tissue repair and tissue regeneration, can be divided into embryonic stem cells (ESCs) and somatic stem cells (SSCs) depending on their origin. As a subpopulation of cells within cancer, cancer stem cells (CSCs) are at the root of therapeutic resistance. Tumor-initiating cells (TICs) are necessary for tumor initiation. Caveolin1 (Cav1), a membrane protein located at the caveolae, participates in cell lipid transport, cell migration, cell proliferation, and cell signal transduction. The purpose of this review was to explore the relationship between Cav1 and stem cells. In ESCs, Cav1 is beneficial for self-renewal, proliferation, and migration. In SSCs, Cav1 exhibits positive or/and negative effects on stem cell self-renewal, differentiation, proliferation, migration, and angiogenic capacity. Cav1 deficiency impairs normal stem cell-based tissue repair. In CSCs, Cav1 inhibits or/and promotes CSC self-renewal, differentiation, invasion, migration, tumorigenicity ability, and CSC formation. And suppressing Cav1 promotes chemo-sensitivity in CSCs and TICs. Cav1 shows dual roles in stem cell biology. Targeting the Cav1-stem cell axis would be a new way for tissue repair and cancer drug resistance.

Breast cancer is one of the most devastating cancers with high morbidity and mortality in females worldwide. Breast tumorigenesis and further development present great uncertainty and complexity, and efficient therapeutic approaches still lack. Accumulating evidence indicates HOX transcript antisense intergenic RNA (HOTAIR) is dysregulated in cancers and has emerged as a novel hotspot in the field. In breast cancer, aberrant HOTAIR expression is responsible for advanced tumor progression by regulating multifarious signaling pathways. Besides, HOTAIR may act as competitive endogenous RNA to bind to several microRNAs and suppress their expressions, which can subsequently upregulate the levels of targeted downstream messenger RNAs, thereby leading to further cancer progression. In addition, HOTAIR works as a promising biomarker and predictor for breast cancer patients’ diagnosis or outcome prediction. Recently, HOTAIR is potentially considered to be a drug target. Here, we have summarized the induction of HOTAIR in breast cancer and its impacts on cell proliferation, migration, apoptosis, and therapeutic resistance, as well as elucidating the underlying mechanisms. This review aims to provide new insights into investigations between HOTAIR and breast cancer development and inspire new methods for studying the association in depth.

Culture of cells in simulated microgravity may be potentially beneficial to the fields of cell biology and somatic cell therapy. We aimed to examine three-dimensional culture condition on pancreatic islets.Islets of Langerhans were cultured in conditions of stasis, microgravity, and microgravity with a polyglycolic acid (PGA) fibrous scaffold. After 5 days in culture, islets were transplanted into the leg muscles of streptozotocin-treated diabetic Wistar rats. The blood glucose and insulin content were determined from the tail vein blood of recipients. The grafts were then frozen, dried, and coated for analysis by scanning electron microscopy.Grafts cultured in the three-dimensional conditions (simulated microgravity in the presence or absence of a PGA fibrous scaffold) were capable of significantly normalizing insulin production and blood glucose concentration when compared to control grafts (p0.017). Scanning electron microscopy showed that the transplanted islets from three-dimensional culture groups demonstrated normal morphology with extracellular matrix on the surface. Islets in the PGA group exhibited well adhesion to PGA scaffolds.The three-dimensional culture conditions significantly improved the function and morphology of the grafts. The function and morphology of the grafts in the microgravity with a scaffold group was the excellent one.

Previous epidemiological studies have shown association between coal burning and human lung cancer. To confirm relationship between coal burning and lung cancer formation and progression the expression of p53 and c-myc in 13 mouse lung cancer induced by coal burning smoke and 5 mouse lung tissue control was studied by DNA-RNA in situ hybridization (ISH). Nine of 13 specimens showed c-myc overexpression but it occurred only 1 of adjacent tissue. There was over pression of p53 mRNA in all 13 lung cancer and 5 adjacent tissue. None in the controls was expression of p53 and c-myc detected. When compared to controls, there was significant higher expression of c-myc gene (P=0.002) and p53 geuc (P=0.0001). The results confirm that overexpression of p53 and c-myc are common molecular events of lung cancer by coal burning smoke and provide further evidence that smoke from coal burning is a causative agent of lung cancer.