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siRNA-dependent KCNMB2 silencing inhibits lung cancer cell proliferation and promotes cell death

Jeong et al. | Nov 01, 2022

siRNA-dependent KCNMB2 silencing inhibits lung cancer cell proliferation and promotes cell death

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.

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Application of gene therapy for reversing T-cell dysfunction in cancer

Hyun Lee et al. | Aug 25, 2022

Application of gene therapy for reversing T-cell dysfunction in cancer

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.

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Extracellular vesicles derived from oxidatively stressed stromal cells promote cancer progression

Chen et al. | Jan 15, 2024

Extracellular vesicles derived from oxidatively stressed stromal cells promote cancer progression

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.

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Down-regulation of CD44 inhibits Wnt/β-catenin mediated cancer cell migration and invasion in gastric cancer

Baek et al. | May 10, 2021

Down-regulation of CD44 inhibits Wnt/β-catenin mediated cancer cell migration and invasion  in gastric cancer

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.

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Inhibiting the ERK pathway and the TRPM7 ion channel in gastric and bladder cancer cells

Yang et al. | Oct 14, 2021

Inhibiting the ERK pathway and the TRPM7 ion channel in gastric and bladder cancer cells

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.

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Conversion of Mesenchymal Stem Cells to Cancer-Associated Fibroblasts in a Tumor Microenvironment: An in vitro Study

Ramesh et al. | Feb 18, 2020

Conversion of Mesenchymal Stem Cells to Cancer-Associated Fibroblasts in a Tumor Microenvironment: An <em>in vitro</em> Study

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.

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Combinatorial treatment by siNOTCH and retinoic acid decreases A172 brain cancer cell growth

Richardson et al. | Nov 14, 2022

Combinatorial treatment by siNOTCH and retinoic acid decreases A172 brain cancer cell growth

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.

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Combating drug resistance in cancer cells: Cooperative effect of green tea and turmeric with chemotherapeutic drug

Nair et al. | Jul 27, 2020

Combating drug resistance in cancer cells: Cooperative effect of green tea and turmeric with chemotherapeutic drug

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.

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Ribosome distribution affects stalling in amino-acid starved cancer cells

Deng et al. | Jan 07, 2022

Ribosome distribution affects stalling in amino-acid starved cancer cells

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.

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Phospholipase A2 increases the sensitivity of doxorubicin induced cell death in 3D breast cancer cell models

Lee et al. | Mar 30, 2022

Phospholipase A2 increases the sensitivity of doxorubicin induced cell death in 3D breast cancer cell models

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.

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