Cell Death Differ: Necrosis apoptosis is not necessary for the development of inflammatory or exudable colon cancer

Colorectal cancer (CRC) is one of the leading causes of cancer-related death worldwide.
, although significant progress has been made in basic genetic research on the disease, genetic susceptivity accounts for only about 20 per cent of CRC cases.
previous studies have shown an increased risk of CRC in patients with inflammatory bowel disease (IBD), so chronic inflammation is also considered a key factor in the development of CRC, and researchers have found that long-term treatment of nonsteroidal anti-inflammatory drugs can reduce the risk of CRC.
although these studies show that the development of CRC does not depend solely on the carcinogenic mutations inherent in tumor cells, the complex mechanisms that regulate tumor-related inflammatory responses are still little known.
necrosis is a form of dissolved programmed cell death that, unlike apoptosis, triggers an inflammatory response.
necrosis are associated with a variety of chronic inflammatory diseases, including inflammatory bowel disease and inflammatory-related cancers.
In the study, where the absence of MLKL or RIPK3 in mouse colitis models led to weight loss, researchers studied the role of necrosis in these gastrointestinal pathology using mouse models of acute colitis, colitis-related CRC, occasional CRC, and spontaneous intestinal tumors.
consistent with previous reports, mice with a lack of end-necrotic apoptosis factor protein MLKL or their activation factor RIPK3 showed more weight loss in the acute colitis model induced by DSS (sodium sulphate Dextran Sulfate Sodium).
, independent repetitive experiments have shown significant changes in the degree of weight loss and accompanying inflammatory pathology associated with Mlkl's absence.
change also provides a possible explanation for previously controversial and contradictory literature.
, contrary to previous reports, the researchers found that the absence of the MLKL gene had no effect on the development of colon cancer in several mouse models.
the absence of MLKL or RIPK3 had no effect on the development of exudable colon cancer overall, these studies do not support the important role of necrosis apoptosis in gastrointestinal inflammation or cancer.
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