Medicines used for cancer treatment often cause serious side effects by damaging normal cells due to nonspecific diffusion. To address this issue, we previously developed an optical method to induce apoptotic cell death via intracellular pH alkalinization using the outward proton pump rhodopsin, Archaerhodopsin-3 (AR3) in various noncancer model cells in vitro and in vivo. In this study, we applied this method to cancer cells and tumors to evaluate its potential as an anticancer therapeutic strategy. First, we confirmed that AR3-expressing murine cancer cell lines (MC38, B16F10) showed apoptotic cell death upon green light irradiation, as indicated by increased levels of cell death and apoptosis-related markers. Next, we established stable AR3-expressing MC38 and B16F10 cells by using viral vectors. When these AR3-expressing cells were subcutaneously transplanted into C57BL/6 mice, the resulting tumors initially grew at a rate comparable to that of control tumors lacking AR3 expression or light stimulation. However, upon green light irradiation, AR3-expressing tumors exhibited either a marked reduction in size or significantly suppressed growth, accompanied by the induction of apoptosis signals and decreased proliferation signals. These results demonstrate that AR3-mediated cell death has potent antitumor effects both in vitro and in vivo. This optical method thus holds promise as a novel cancer therapy with potentially reduced side effects.

Cancer cells often contain an abnormal number of chromosomes as a result of incorrect chromosome segregation during cell division.

These fragments of genetic material can be encapsulated by a membrane, forming small nucleus-like structures called micronuclei. These structures often rupture, exposing chromatin (DNA and associated proteins) to the harsh environment of the cytoplasm, which can lead to large-scale DNA damage in a process called chromothripsis, or chromosome shattering and scrambling.

In a new Science study, researchers report that the cytoplasmic protein NEDD4-binding protein 2 may be responsible for chromothripsis.

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A protein that cuts double-stranded DNA contributes to chromosome scrambling in human cancer cells.

Stanley Clarke and Marcin Imieliński Authors Info & Affiliations

Among survivors of non-small cell lung cancer, nearly 8% developed non-lung secondary cancers over about 6 years, and this risk may be driven by genetic factors.

A new genome-wide mapping method finally shows how thousands of genes connect to drive disease.

A new study from the MRC Laboratory of Medical Sciences (LMS) in London, UK reveals how ancient viral DNA once written off as “junk” plays a crucial role in the earliest moments of life. The research, published in Science Advances, begins to untangle the role of an ancient viral DNA element called MERVL in mouse embryonic development and provides new insights into a human muscle wasting disease.

Transposable elements are stretches of DNA that can move around the genome. Many of these DNA sequences originate from long ago, when viruses inserted their genetic material into our ancestors’ genomes during infection. Today, these viral transposable elements make up around 8–10% of the mammalian genome.

Once disregarded as “junk” DNA, we now know that many transposable elements play an important role in influencing how genes are turned on and off, especially during early development. They have a variety of beneficial and harmful roles in the body, for example, some help regulate normal immune responses, while others can disrupt genes and contribute to diseases like cancer.