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.

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.

In this study, we aimed to characterize CD44-mediated regulation of the Wnt/β-catenin signaling pathway, which promotes cancer invasion and metastasis. We hypothesized that CD44 down-regulation will inhibit gastric cancer cell migration and invasion by leading to down-regulation of Wnt/β-catenin signaling. We found that CD44 up-regulation was significantly related to poor prognosis in gastric cancer patients. We demonstrated the CD44 down-regulation decreased β-catenin protein expression level. Our results suggest that CD44 down-regulation inhibits cell migration and invasion by down-regulating β-catenin expression level.

In this work the authors investigate new possible treatment methods for gastric and bladder cancers. They specifically targeted the transient receptor potential cation subfamily M member 7 (TRPM7), an ion channel that plays an important role in the survival of both of these cancers, and extracellular regulated kinases (ERKs),which contributes to the carcinogenesis of many cancers including gastric cancer. As a result, the authors consider the effects of Ginsenoside Rd, NS8593, curcumin, and icariin , known to inhibit TRPM7 and ERK. The authors found that these treatments decrease proliferation and induce apoptosis in studies of gastric and bladder cancer cells.

Mesenchymal stem cells(MSCs) play a role in tumor formation by differentiating into cancer associated fibroblasts (CAFs) which enable metastasis of tumors. The process of conversion of MSCs into CAFs is not clear. In this study, authors tested the hypothesis that cancers cells secrete soluble factors that induce differentiation by culturing bone marrow mesenchymal stem cells in media conditioned by a breast cancer cell line.

Treatments inhibiting Notch signaling pathways have been explored by researchers as a new approach for the treatment of glioblastoma tumors, which is a fast-growing and aggressive brain tumor. Recently, retinoic acid (RA) therapy, which inhibits Notch signaling, has shown a promising effect on inhibiting glioblastoma progression. RA, which is a metabolite of vitamin A, is very important in embryonic cellular development, which includes the regulation of multiple developmental processes, such as brain neurogenesis. However, high doses of RA treatment caused many side effects such as headaches, nausea, redness around the injection site, or allergic reactions. Therefore, we hypothesized that a combination treatment of RA and siRNA targeting NOTCH1 (siNOTCH1), the essential gene that activates Notch signaling, would effectively inhibit brain cancer cell proliferation. The aim of the study was to determine whether inhibiting NOTCH1 would inhibit the growth of brain cancer cells by cell viability assay. We found that the combination treatment of siNOTCH1 and RA in low concentration effectively decreased the NOTCH1 expression level compared to the individual treatments. However, the combination treatment condition significantly decreased the number of live brain cancer cells only at a low concentration of RA. We anticipate that this novel combination treatment can provide a solution to the side effects of chemotherapy.

The major drawback of chemotherapy regimens for treating cancer is that the cancerous cells acquire drug resistance and become impervious to further dose escalation. Keeping in mind the studied success of herbal formulations with regard to alternative treatments for cancer, we hypothesized that the use of a chemotherapeutic drug and proprietary herbal formulation, HF1, would combat this phenomenon when administered with common chemotherapeutic drug 5FU. Results demonstrated a cooperative effect between HF1 and 5FU on the drug resistant cell line, implying that administration of HF1 with 5FU results in cell death as measured by MTT assay.

In this article, the authors analyzed ribosome profiling data from amino acid-starved pancreatic cancer cells to explore whether the pattern of ribosome distribution along transcripts under normal conditions can predict the degree of ribosome stalling under stress. The authors found that ribosomes in amino acid-deprived cells stalled more along elongation-limited transcripts. By contrast, they observed no relationship between read density near start and stop and disparities between mRNA sequencing reads and ribosome profiling reads. This research identifies an important relationship between read distribution and propensity for ribosomes to stall, although more work is needed to fully understand the patterns of ribosome distribution along transcripts in ribosome profiling data.

Inefficient penetration of cancer drugs into the interior of the three-dimensional (3D) tumor tissue limits drugs' delivery. The authors hypothesized that the addition of phospholipase A2 (PLA2) would increase the permeability of the drug doxorubicin for efficient drug penetration. They found that 1 mM PLA2 had the highest permeability. Increased efficiency in drug delivery would allow lower concentrations of drugs to be used, minimizing damage to normal cells.

The current five-year survival rate of metastasized prostate cancer is only 30% and occurs in every one in nine men. Researchers have shown that people with a type of dwarfism called Laron’s Syndrome are immune to cancer due to their low levels of insulin-like growth factor-1 (IGF-1). For this reason, experimentally modifying the level of IGF-1 could provide better insight into whether lowering the levels of IGF-1 in prostate cancer cell lines (e.g. PC-3) could be an effective treatment to reduce their rates of proliferation and migration and increase apoptosis. We selected three compounds, which researchers have shown decrease IGF-1 levels, to test and combine to determine which is the most promising.