Asthma affects over 334 million people worldwide and is triggered by inhalation of environmental stimuli. The authors of this study characterized the effect of exposure to common spoilage yeast, Pichia kidriavzevii on alveolar epithelial cells. A direct correlation between infection duration and asthmatic status of these cells was found, indicating the potential for this yeast to be an environmental stimulus of asthma and warranting further study.

The authors compare RNA expression profiles across three human cell types following infection with MERS-CoV

This paper hypothesized that the tumor microenvironment mediates cancer’s response to oxidative stress by delivering extracellular vesicles to cancer cells. Breast and lung cancer cells were treated with EVs, reavealing that EVs extracted from oxidatively stressed adipocytes increased the cell proliferation of breast cancer cells. These findings present a novel way that the TME influences cancer progression.

Tertiary lymphoid structures (TLS) are lymph node-like structures that form at sites of inflammation, and their presence in cancer patients is predictive of a better clinical outcome. One significant obstacle to TLS formation is reduced immune cell infiltration into the tumor microenvironment (TME). Recent studies have shown that vasculature normalizing (VN) agents may override this defect to improve tissue perfusion and increased immune cell entry into the TME. However, their effects on immune cell and tumor cell phenotype remain understudied. Here the authors investigate whether treating tumor cells with VN would reduce their immunosuppressive phenotype and promote production of chemokine that recruit immune cells and foster TLS formation.

Here, seeking to better understand the genetic associations underlying non-small cell lung cancer, the authors screened hundreds of genes, identifying that KCNMB2 upregulation was significantly correlated with poor prognoses in lung cancer patients. Based on this, they used small interfering RNA to decrease the expression of KCNMB2 in A549 lung cancer cells, finding decreased cell proliferation and increased lung cancer cell death. They suggest this could lead to a new potential target for lung cancer therapies.

The purpose of this study was to test the anti-cancer properties and pro-apoptotic effects of the polyherbal formulation MAT20 as a complementary treatment. Moringa oleifera (Moringa), Phyllanthus emblica (Amla) and Ocimum sanctum (Tulsi), these 3 herbs were used to formulate MAT20, which contain phytochemicals that are known to display anti-cancer properties. In this study, we hypothesized that MCF-7 breast cancer cells treated with MAT20 would show increased cytotoxicity compared to its individual plant extracts.

In South Asian countries, the major cause of oral cancer is reported to be chewing paan, which is comprised of betel leaf daubed with slaked lime paste and areca nut. To investigate how paan may contribute to the onset of cancer, the authors treated two immortalized cell lines with extracts of betel leaf, areca nut, and lime and evaluated how these treatments affected cell proliferation and cell death. Initial results indicate that while betel leaf alone may inhibit cell growth, areca nut promoted cancer cell survival and proliferation, even when co-treated with betel leaf. These data suggest that areca nut could exacerbate the progression of oral cancer in humans.

Stem cells are at the forefront of research in regenerative medicine and cell therapy. Two essential properties of stem cells are self-renewal and potency, having the ability to specialize into different types of cells. Here, Park and Jeong took advantage of previously identified stem cell transcription factors associated with potency to differentiate umbilical cord mesenchymal stem cells (US-MSCs) from morphologically similar fibroblasts. Western blot analysis of the transcription factors Klf4, Nanog, and Sox2 revealed their expression was unique to US-MSCs providing insight for future methods of differentiating between these cell lines.

Since cancer cells inhibit T-cell activity, the authors investigated a method to reverse T-cell disfunction with gene therapy, so that the T-cells would become effective once again in fighting cancer cells. They used the inhibition of proprotein convertases (PCSK1) in T cells and programmed death-ligand 1 (CD274) in cancer cells. They observed the recovery of IL-2 expression in Jurkat cells, with increased recovery noted in a co-culture sample. This study suggests a novel strategy to reactivate T cells.

Cellular senescence plays a key role in aging cells and is attributed to a number of disease and pathology. These authors find that genetic editing of both RPS6KB1 and PPARGC1A revitalizes a human skin fibroblast cell line.