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Cancer Cells and Bacterial Resistance: How the CRISPR-Cas9 System Targets and Destroys Tumor Cells

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Research has shown that one high -intensity movement can effectively suppress breast cancer cell growth. In particular, the higher the motor strength, the greater the anticancer effect, and it was argued that the exercise should be considered as a core treatment beyond the auxiliary therapy.

A research team at the Australian Eddis Koan University announced on the 12th that a study of 32 survivors of breast cancer analyzed the impact of single exercise sessions on cancer cells. The findings were published in the international journal The Treatment and Research of Breast Cancer. The team divided the participants into a strength exercise group and a high -intensity interval movement group for 45 minutes, and then collected and analyzed blood before and after exercise. Both groups conducted a high intensity movement of at least 7-8 out of 10 out of 10.

The research team was administered to breast cancer cells cultured in the laboratory, and cancer cells exposed to blood after exercise stopped or died. On the other hand, cancer cells that administered blood before exercise have not changed. The blood of the strength exercise group inhibited cancer cell growth by 21%, and the high -strength interval movement group inhibited up to 29%.

This effect was analyzed because of the Myokine, a protein secreted by muscles during exercise. Myokine consists of about 200 kinds of hormones and has a variety of positive effects, including inflammation control and immune response. In the blood after exercise, the level of anticancer myokine, such as decorin, interukin-6 and spark, increased by 47%. In particular, the higher the interleukin-6 levels involved in the immune response, the larger the cancer cell suppression effect, which increased the most after the high-intensity interval movement.

But not all exercises have the same effect. Professor Robert Newton, who led the research, said, “The stronger the stimulus, the more active the anti -cancer Myokine secretion is.”

The anticancer effect of exercise is also proven in other studies. According to a study published in the New England Journal in June, the survivors of the long -intensity movement were 37% lower than the group that did not. Professor Newton emphasized that “exercise should no longer be recognized as an additional activity of existing chemotherapy, but a key primary treatment for cancer patients.” However, cancer patients have a variety of cancer types and health, so they need to consult with a specialist before starting the exercise.

By Hyun Soo -ah, reporter [email protected]

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Cancer cells and Bacterial Resistance: How the CRISPR-Cas9 System Targets and Destroys Tumor Cells

Understanding the Unexpected Link: Cancer, Bacteria, and Resistance

For years, cancer treatment has focused primarily on directly targeting cancerous cells. However, emerging research reveals a surprising connection between cancer progress and the microbiome – the community of bacteria living within us. Certain bacteria can promote tumor growth, while others can enhance the effectiveness of cancer therapies. Critically, bacteria can also develop resistance mechanisms, mirroring those seen in antibiotic resistance, which can then shield cancer cells from treatment. This interplay necessitates innovative approaches, and CRISPR-Cas9 gene editing is rapidly becoming a powerful tool in this fight. This article explores how CRISPR-Cas9 is being leveraged to overcome these challenges, focusing on tumor microenvironment modulation and direct cancer cell destruction.

The Role of the Tumor Microenvironment & Bacterial Influence

The tumor microenvironment (TME) is a complex ecosystem surrounding a tumor, comprising blood vessels, immune cells, fibroblasts, and, importantly, bacteria. bacteria within the TME can:

* Promote Inflammation: Chronic inflammation is a hallmark of cancer and fuels tumor progression. Certain bacterial species exacerbate this inflammation.

* Suppress Immune Response: Some bacteria actively suppress the immune system, preventing it from recognizing and attacking cancer cells. Immune checkpoint inhibitors are frequently enough less effective in patients with specific bacterial profiles.

* Metabolic Alterations: Bacteria can alter the metabolic landscape of the TME, providing nutrients to cancer cells and enhancing their growth.

* Drug Resistance: Bacteria can metabolize chemotherapy drugs, reducing their efficacy, or even transfer resistance genes to cancer cells. This is a growing concern in chemotherapy resistance cases.

Understanding these bacterial contributions is crucial for developing effective cancer therapies. Microbiome analysis is becoming increasingly important in personalized cancer treatment.

CRISPR-Cas9: A Revolutionary gene Editing Tool

CRISPR-Cas9 (clustered Regularly Interspaced Short Palindromic Repeats and CRISPR-associated protein 9) is a revolutionary gene editing technology derived from a bacterial defense mechanism.It allows scientists to precisely target and modify DNA sequences. Here’s how it works:

  1. Guide RNA (gRNA) Design: A short RNA sequence (gRNA) is designed to match the specific DNA sequence you want to target.
  2. Cas9 Enzyme: The Cas9 enzyme acts like molecular scissors, guided by the gRNA to the target DNA.
  3. DNA Cleavage: Cas9 cuts the DNA at the targeted location.
  4. Cellular Repair Mechanisms: The cell’s natural repair mechanisms kick in. these can be harnessed to either disrupt the gene (gene knockout) or insert a new gene (gene editing).

Targeting Cancer Cells Directly with CRISPR-Cas9

CRISPR-Cas9 can be used to directly target and destroy cancer cells by:

* Disrupting Oncogenes: Oncogenes are genes that promote cancer growth. CRISPR-Cas9 can be used to disable these genes, halting tumor progression. Examples include targeting KRAS, EGFR, and MYC.

* Restoring Tumor Suppressor Genes: Tumor suppressor genes normally prevent cancer development. CRISPR-Cas9 can be used to repair or reactivate these genes. TP53 is a frequently mutated tumor suppressor gene targeted by this approach.

* Inducing Apoptosis: Programmed cell death (apoptosis) is a natural process that eliminates damaged cells. CRISPR-Cas9 can be used to activate apoptosis pathways in cancer cells.

* Enhancing Immunogenicity: Modifying cancer cells with CRISPR-Cas9 to express more antigens can make them more visible to the immune system, boosting the effectiveness of immunotherapy.

Combating Bacterial Resistance in the Tumor Microenvironment

CRISPR-Cas9 isn’t limited to targeting cancer cells themselves. It can also be used to address the bacterial component of the TME:

* Targeting Antibiotic Resistance Genes: CRISPR-Cas9 can be designed to specifically target and destroy antibiotic resistance genes within bacteria in the TME, restoring sensitivity to antibiotics and perhaps enhancing chemotherapy efficacy.

* Modulating Bacterial Composition: By selectively eliminating bacteria that promote tumor growth and encouraging the growth of beneficial bacteria, CRISPR-Cas9 can reshape the microbiome to favor anti-cancer immunity. This is a form of microbiome engineering.

* Disrupting Bacterial Virulence Factors: CRISPR-Cas9 can target genes responsible for bacterial virulence – the factors that allow bacteria to cause harm – reducing their ability to promote cancer progression.

Delivery Challenges and Advancements

Delivering CRISPR-Cas9 to the target cells remains a meaningful challenge. Current delivery methods include:

* Viral Vectors: Modified viruses (e.g., adeno-associated viruses – AAVs) are commonly used to deliver CRISPR-Cas9 components. However, they

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