Researchers from Wenzhou Medical University in China have identified a mechanism involving long non-coding RNAs (lncRNA) that contributes to colorectal cancer (CRC) progression. CRC is the third most common cancer worldwide and is one of the most lethal cancers across the globe. Understanding the molecular mechanisms that underlie the development and progression of CRC is critical to developing biomarkers to detect it and new therapeutics to treat it.
In recent years, non-coding RNAs—especially microRNAs (miRNAs) and long non-coding RNAs (lncRNAs)—have emerged as powerful regulators of cellular behavior. These molecules modulate gene expression, often by targeting mRNAs for translational suppression or degradation. Two recent studies—one focused on osteoarthritis and the other on 5-Fu-resistant colorectal cancer—illustrate how these non-coding, regulatory RNAs operate within disease-relevant signaling networks, providing new points for therapeutic intervention.
Both studies use the pmirGLO Dual-Luciferase miRNA Target Expression Vector to evaluation predicted miRNA activity. This dual-luciferase system offers a clean and quantifiable way to validate miRNA–mRNA interactions using a simple bioluminescent readout. By cloning the 3´ untranslated regions (UTRs) of suspected targets downstream of a firefly luciferase reporter and normalizing against Renilla luciferase, researchers can rapidly confirm whether a miRNA directly regulates its target.
Traditionally, RNA methylation has been studied in the context of gene expression regulation, RNA stability and translation efficiency, with its primary role thought to be in modulating cellular homeostasis and protein synthesis. However, a 2025 study by Dharmadkikari and colleagues uncovers an unexpected and critical function for RNA methylation in mitotic spindle integrity.
False color transmission electron microscope (TEM) micrograph of a mitotic cell in metaphase stage showing chromosomes (purple) in the equatorial plane and one of the mitotic spindle poles (blue).
The study identifies a critical role for SPOUT1/CENP-32-dependent methylation in mitotic spindle formation and accurate chromosome segregation. Originally identified in a large-scale analysis of proteins associated with mitotic chromosomes, SPOUT1/CENP-32 encodes a putative RNA methyltransferase. The protein localizes to mitotic spindles, and when it is absent centrosome detachment from the spindle poles, delayed anaphase, and chromosome segregation errors are observed. Further, CRISPR experiments in human cells show that the protein is essential for cell viability.
Post-translational modifications of proteins are critical for proper protein function. Modifications such as phosphorylation/dephosphorylation can act as switches that activate or inactivate proteins in signaling cascades. The addition of specific sugars to membrane proteins on cells are critical for recognition, interaction with the extracellular matrix and other activities. While we know volumes about some types of protein modifications, ADP-ribosylation on aspartate and glutamate residues has been more difficult to study because of the chemical instability of these ester-linked modifications.
Matić Lab (Eduardo José Longarini and Ivan Matić) recently published a study that explored mono-ADP-ribosylation (ADPr) on aspartate and glutamate residues by the protein PARP1 and its potential reversal by PARG. PARP1 and PARG signaling are central to DNA repair and apoptosis pathways, making them potentially powerful therapeutic targets in cancer or neurodegenerative diseases in which DNA repair processes are often disrupted.
Since the COVID-19 pandemic, public health researchers and research scientists have sought more urgently to understand the worldwide respiratory virus landscape. The COVID-19 pandemic has forced us to re-evaluate our global public health priorities and activities. Additionally, acute respiratory tract infections are one of the leading causes of illness and death worldwide, particularly in developing countries. To really understand what changed with the pandemic and how we can best respond going forward, we need to understand what the baseline landscape was before the pandemic. Studies using samples that were collected prior to the pandemic are essential to this effort.
The Mozambique Channel, which is located between the Madagascar and Mozambique on the African coast, is an important hot spot for biodiversity because its many coastal ecosystems provide a range of habitats that support diverse plant and animal species. Understanding the biodiversity of an ecosystem, particularly biodiversity hot spots, is important for many reasons. For marine systems, accurate classification and reporting of fish species supports fisheries research, natural resource surveys, forensic studies, conservation studies, and enables discovery of new or under-reported species. Studies have been limited along the west coast of Africa and are only now in their early stages.
A 2024 research study by Muhala and colleagues applied DNA barcoding to evaluate the composition of marine and coastal fish diversity from the Mozambican coast. In the study, the Wizard® Genomic DNA Purification Kit was used to extract DNA from both teleost (ray-finned) and elasmobranch (sharks, rays and skates) fish classes, with a total of 143 species sampled from local artisanal fisheries along the Mozambican coast. The samples were primarily composed of muscle or fin tissues, which are ideal for genetic analysis due to their higher DNA yield. These tissue samples were collected from various fish species captured along the coast of Mozambique, stored in ethanol (96%) to preserve DNA integrity, and then processed using the Wizard kit. Total genomic DNA was extracted from the muscle or fin tissues, as per the manufacturer’s protocol. This method ensures the isolation of high-quality genomic DNA, which is crucial for subsequent polymerase chain reaction (PCR) amplification and sequencing. The COI gene (cytochrome c oxidase subunit I) was targeted for DNA barcoding, enabling species identification and assessment of genetic diversity.
Almost three-quarters of the major crop plants across the globe depend on some kind of pollinator activity, and over one-third of the worldwide crop production is affected by bees, birds, bats, and other pollinators such as beetles, moths and butterflies (1). The economic impact of pollinators is tremendous: Between $235–577 billion dollars of global annual food production relies on the activity of pollinators (2). Nearly 200,000 species of animals act as pollinators, including some 20,000 species of bees (1). Some of the relationships between pollinators and their target plants are highly specific, like that between fig plants and the wasps that pollinate them. Female fig wasps pollinate the flowers of fig plants while laying their eggs in the flower. The hatched wasp larvae feed on some, but not all, of the seeds produced by fertilization. Most of the 700 fig plants known are each pollinated by only one or a few specific wasp species (3). These complex relationships are one reason pollinator diversity is critical.
Measuring the Success of Conservation Legislation
A bee pollinates the lavender flowers.
We are now beginning to recognize how critical pollinator diversity is to our own survival, and many governments, from the local level to the national level are enacting policies and legislation to help protect endangered or threatened pollinator species. However, ecosystems and biodiversity are complex subjects that make measuring and attributing meaningful progress on conservation difficult. Not only are there multiple variables in every instance, but determining the baseline starting point before the legislation is difficult. However, there are dramatic examples of success in saving species through legislative and regulatory action. The recovery of the bald eagle and other raptor populations in the United States after banning the use of DDT is one such example (4).
Approximately 30 million years ago, a retrovirus integrated into the germline of a common ancestor of baboons, gorillas, chimpanzees and humans. That endogenous retrovirus, now known as gammaretrovirus human endogenous retrovirus 1 (HERV-1), may provide clues about the aberrant regulation of gene transcription that enables tumor cells to grow and survive.
Understanding the Mechanism Behind Cancer Gene Expression
Scientists have long described the striking differences in gene expression, signaling activity and metabolism between cancer cells and normal cells, but the underlying mechanisms that cause these differences are not fully understood. In a recent Science Advancesarticle, published by Ivancevic et al., researchers from the University of Colorado, Boulder; the University of Colorado Anschutz Medical Campus, and the University of Colorado School of Medicine report their efforts to identify endogenous retrovirus elements that might be part of the answer to the complex question of what biological events are responsible for the changes in gene expression in cancer cells.
The researchers hypothesized that transposable elements (TEs), specifically those associated with endogenous retroviruses could be involved in cancer-specific gene regulation. Endogenous retroviruses (ERVs) are the remnants of ancient retroviral infections that have integrated into the germline of the host.
Identifying Endogenous Retrovirus Elements That Affect Cancer Gene Expression
There is no shortage of stories about great scientific collaborations that have taken root as the result of an excited conversation between two scientists over sandwiches and beer at a bar or a deli. One of the most famous examples of such a conversation was that between Herbert Boyer and Stanley Cohen when they attended a conference on bacterial plasmids in 1972—that very conversation led to the formation of the biotechnology field as the two scientists worked together to clone specific regions of DNA (1).
“Over hot pastrami and corned beef sandwiches, Herbert Boyer and Stanley Cohen opened the door to genetic engineering and laid the foundations for gene therapy and the biotechnology industry.”
Steven Johnson, author of Where Do Good Ideas Come From, credits the English coffee house as being crucial to the spread of the enlightenment movement in the 17th and 18th centuries (2). He argues that coffee houses provide a space where ideas can come together and form networks. In fact, he defines the concept of “idea” not as a single entity—a grand thought that poofs into existence upon hard work—but at its simplest level, a new idea is a new network of neurons firing in sync with each other.
Johnson further argues that the development of great new ideas not only requires a space for ideas to bump into each other, connect and form a network, but also that great ideas are rarely the product of a single “Eureka” moment. Rather, they are slowly developing, churning hunches that have very long incubation periods (2).
At the American Association for Cancer Research meeting in April 2016, then Vice President of the United States, Joe Biden, revealed the Cancer Moonshot℠ initiative— a program with the goals of accelerating scientific discovery in cancer research, fostering greater collaboration among researchers, and improving the sharing of data (1,2). The Cancer Moonshot is part of the 21st Century Cures Act, which earmarked $1.8 billion for cancer-related initiatives over 7 years. The National Cancer Institute (NCI) and the Cancer Moonshot program have supported over 70 programs and consortia, and more than 250 research projects. According to the NCI, the initiative from 2017 to 2021 resulted in over 2,000 publications, 49 clinical trials and more than 30 patent filings. Additionally, the launch of trials.cancer.gov has made information about all cancer research trials accessible to anyone who needs it (3).
“We will build a future where the word ‘cancer’ loses its power.”
First Lady, Dr. Jill Biden
In February 2022, the Biden White House announced a plan to “supercharge the Cancer Moonshot as an essential effort of the Biden-Harris administration” (4). Biden noted in his address that, in the 25 years following the Nixon administration’s enactment of the National Cancer Act in 1971, significant strides were made in understanding cancer. It is now recognized not as a single disease, but as a collection comprising over 200 distinct diseases. This period also saw the development of new therapies and enhancements in diagnosis. However, despite a reduction in the cancer death rate by more than 25% over the past 25 years, cancer continues to be the second leading cause of death in the United States [4].
The Cancer Moonshot is a holistic attempt to improve access to information, support and patient experiences, while fostering the development of new therapeutics and research approaches to studying cancer. In this article, we will focus on research, diagnostics and drug discovery developments.
Solving for Undruggable Targets
KRAS , a member of the RAS family, has long been described as “undruggable” in large part because it is a small protein with a smooth surface that does not present many places for small molecule drugs to bind. The KRAS protein acts like an off/on switch depending upon whether it has GDP or GTP bound. KRAS mutations are associated with many cancers including colorectal cancer (CRC), non-small cell lung cancer (NSCLC), and pancreatic ductal adenocarcinoma (PDAC). The G12 position in the protein is the most commonly mutated; G12C accounts for 13% of the mutations at this site, and is the predominant substitution found in NSCLC, while G12D is prevalent in PDAC (5).
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