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Reducing KAT7 expression inhibits colorectal cancer progression<\/h1>Gastrointestinal Disorders<\/a>, Featured Articles<\/a> <\/span><\/span><\/header>\n<\/div><\/section>
\nColorectal cancer background and risk factors
\nColorectal (or bowel) cancer (CRC) is cancer anywhere in the colon (the large intestine) or the rectum.<\/h3>\n
<\/p>\n
Colorectal cancer background and risk factors<\/h4>\nColorectal (or bowel) cancer (CRC) is cancer anywhere in the colon (the large intestine) or the rectum. According to Cancer Research UK [1], for the latest time frame that we have statistics for (2017\u20132019), there are around 44 100 new cases of CRC in the UK every year. In the UK, the incidence is slightly higher in men than women, and it is the third most common cancer for both sexes: after breast cancer and lung cancer in females; and after prostate cancer and lung cancer in males [2]. Non-modifiable risk factors for bowel cancer include age and genetics; however, 54% of CRC cases in the UK are preventable, with modifiable risk factors including eating processed meat, obesity and overweight, drinking alcohol, smoking, too little physical activity and eating too little fibre.<\/p>\n<\/div><\/section>
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\nCRC screening, diagnosis and treatment<\/h4>\n
CRC screening every 2 years by fecal immunochemical test (FIT) is offered to everyone in Scotland from the age of 50\u201374, and in England the age limit has just been extended to include everyone in the age 50\u201352 range from mid-January 2025, bringing England in line with the UK National Screening Committee\u2019s age recommendation. Following a positive FIT test, the diagnosis pathway involves colonoscopy, then CT or MRI scans to ascertain spread of the disease and genetic testing to help determine the treatment plan. The genetic testing involves checking for mutations in the RAS and BRAF genes, as well as microsatellite instability\/ DNA mismatch repair status. Treatment depends on the stage of the cancer: surgery for grade 1; surgery and chemotherapy for grades 2 and 3; and the options for grade 4 cancer include surgery, chemotherapy, radiotherapy, immunotherapy and targeted cancer drugs. However, despite advances in treatment, 5- and 10-year survival rates for advanced CRC are still poor. The development of drug resistance is a major factor in these low survival rates and is a driver for the search for new possible therapeutic targets.<\/p>\n
KAT7: possible new therapeutic target<\/h4>\n
As we have discussed previously in these pages, mutations in the enzymes responsible for the epigenetic modifications of DNA methylation and histone acetylation play an important role in cancer progression. One such protein that has come under scrutiny is the histone acetyltransferase, KAT7, modifying H3 and H4 histones. Recent studies have shown that KAT7 plays a role in the early stages of lung adenocarcinoma, aggressive development of liver cancer, worse prognosis in head and neck squamous cell carcinoma and CRC. A recent paper by Wang et al. has investigated the expression of KAT7 in CRC patients and its correlation with prognosis [3]. They found that upregulated KAT7 was associated with poor prognosis and that knockdown of the protein increased apoptosis and inhibited proliferation, migration and invasion of CRC cells. They found that KAT7 acetylation of histone H3 enhances MRAS gene transcription, which activates the MAPK\/ERK pathway to promote malignant CRC. Hence, not only would assessment of KAT7 expression be useful in CRC prognostication, but they conclude that it represents a promising target for CRC therapy. Although, of course, further work is needed, the addition of new targets for treating CRC can only be good news for improving survival rates.<\/p>\n
References:<\/strong><\/em>
\n 1. Bowel cancer statistics [webpage]. Cancer Research UK (https:\/\/shorturl.at\/TfJQN<\/a>).<\/em>
\n 2. Cancer incidence for common cancers [webpage]. Cancer Research UK (https:\/\/shorturl.at\/SioUv<\/a>).<\/em>
\n 3. Wang H, Guan T, Hu R et al. Targeting KAT7 inhibits the progression of colorectal cancer. Theranostics 2025;15(4):1478\u20131495 (https:\/\/www.thno.org\/v15p1478.htm<\/a>).<\/em><\/p>\n<\/div><\/section>
\n
Colorectal cancer background and risk factors
\nColorectal (or bowel) cancer (CRC) is cancer anywhere in the colon (the large intestine) or the rectum.<\/h3>\n
<\/p>\n
Colorectal cancer background and risk factors<\/h4>\nColorectal (or bowel) cancer (CRC) is cancer anywhere in the colon (the large intestine) or the rectum. According to Cancer Research UK [1], for the latest time frame that we have statistics for (2017\u20132019), there are around 44 100 new cases of CRC in the UK every year. In the UK, the incidence is slightly higher in men than women, and it is the third most common cancer for both sexes: after breast cancer and lung cancer in females; and after prostate cancer and lung cancer in males [2]. Non-modifiable risk factors for bowel cancer include age and genetics; however, 54% of CRC cases in the UK are preventable, with modifiable risk factors including eating processed meat, obesity and overweight, drinking alcohol, smoking, too little physical activity and eating too little fibre.<\/p>\n<\/div><\/section>
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<\/span><\/span><\/div>
\n<\/div><\/div><\/div>
\n<\/span><\/span><\/div>
\nCRC screening, diagnosis and treatment<\/h4>\n
CRC screening every 2 years by fecal immunochemical test (FIT) is offered to everyone in Scotland from the age of 50\u201374, and in England the age limit has just been extended to include everyone in the age 50\u201352 range from mid-January 2025, bringing England in line with the UK National Screening Committee\u2019s age recommendation. Following a positive FIT test, the diagnosis pathway involves colonoscopy, then CT or MRI scans to ascertain spread of the disease and genetic testing to help determine the treatment plan. The genetic testing involves checking for mutations in the RAS and BRAF genes, as well as microsatellite instability\/ DNA mismatch repair status. Treatment depends on the stage of the cancer: surgery for grade 1; surgery and chemotherapy for grades 2 and 3; and the options for grade 4 cancer include surgery, chemotherapy, radiotherapy, immunotherapy and targeted cancer drugs. However, despite advances in treatment, 5- and 10-year survival rates for advanced CRC are still poor. The development of drug resistance is a major factor in these low survival rates and is a driver for the search for new possible therapeutic targets.<\/p>\n
KAT7: possible new therapeutic target<\/h4>\n
As we have discussed previously in these pages, mutations in the enzymes responsible for the epigenetic modifications of DNA methylation and histone acetylation play an important role in cancer progression. One such protein that has come under scrutiny is the histone acetyltransferase, KAT7, modifying H3 and H4 histones. Recent studies have shown that KAT7 plays a role in the early stages of lung adenocarcinoma, aggressive development of liver cancer, worse prognosis in head and neck squamous cell carcinoma and CRC. A recent paper by Wang et al. has investigated the expression of KAT7 in CRC patients and its correlation with prognosis [3]. They found that upregulated KAT7 was associated with poor prognosis and that knockdown of the protein increased apoptosis and inhibited proliferation, migration and invasion of CRC cells. They found that KAT7 acetylation of histone H3 enhances MRAS gene transcription, which activates the MAPK\/ERK pathway to promote malignant CRC. Hence, not only would assessment of KAT7 expression be useful in CRC prognostication, but they conclude that it represents a promising target for CRC therapy. Although, of course, further work is needed, the addition of new targets for treating CRC can only be good news for improving survival rates.<\/p>\n
References:<\/strong><\/em>
\n 1. Bowel cancer statistics [webpage]. Cancer Research UK (https:\/\/shorturl.at\/TfJQN<\/a>).<\/em>
\n 2. Cancer incidence for common cancers [webpage]. Cancer Research UK (https:\/\/shorturl.at\/SioUv<\/a>).<\/em>
\n 3. Wang H, Guan T, Hu R et al. Targeting KAT7 inhibits the progression of colorectal cancer. Theranostics 2025;15(4):1478\u20131495 (https:\/\/www.thno.org\/v15p1478.htm<\/a>).<\/em><\/p>\n<\/div><\/section>
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CRC screening, diagnosis and treatment<\/h4>\n
CRC screening every 2 years by fecal immunochemical test (FIT) is offered to everyone in Scotland from the age of 50\u201374, and in England the age limit has just been extended to include everyone in the age 50\u201352 range from mid-January 2025, bringing England in line with the UK National Screening Committee\u2019s age recommendation. Following a positive FIT test, the diagnosis pathway involves colonoscopy, then CT or MRI scans to ascertain spread of the disease and genetic testing to help determine the treatment plan. The genetic testing involves checking for mutations in the RAS and BRAF genes, as well as microsatellite instability\/ DNA mismatch repair status. Treatment depends on the stage of the cancer: surgery for grade 1; surgery and chemotherapy for grades 2 and 3; and the options for grade 4 cancer include surgery, chemotherapy, radiotherapy, immunotherapy and targeted cancer drugs. However, despite advances in treatment, 5- and 10-year survival rates for advanced CRC are still poor. The development of drug resistance is a major factor in these low survival rates and is a driver for the search for new possible therapeutic targets.<\/p>\n
KAT7: possible new therapeutic target<\/h4>\n
As we have discussed previously in these pages, mutations in the enzymes responsible for the epigenetic modifications of DNA methylation and histone acetylation play an important role in cancer progression. One such protein that has come under scrutiny is the histone acetyltransferase, KAT7, modifying H3 and H4 histones. Recent studies have shown that KAT7 plays a role in the early stages of lung adenocarcinoma, aggressive development of liver cancer, worse prognosis in head and neck squamous cell carcinoma and CRC. A recent paper by Wang et al. has investigated the expression of KAT7 in CRC patients and its correlation with prognosis [3]. They found that upregulated KAT7 was associated with poor prognosis and that knockdown of the protein increased apoptosis and inhibited proliferation, migration and invasion of CRC cells. They found that KAT7 acetylation of histone H3 enhances MRAS gene transcription, which activates the MAPK\/ERK pathway to promote malignant CRC. Hence, not only would assessment of KAT7 expression be useful in CRC prognostication, but they conclude that it represents a promising target for CRC therapy. Although, of course, further work is needed, the addition of new targets for treating CRC can only be good news for improving survival rates.<\/p>\n
References:<\/strong><\/em>
\n 1. Bowel cancer statistics [webpage]. Cancer Research UK (https:\/\/shorturl.at\/TfJQN<\/a>).<\/em>
\n 2. Cancer incidence for common cancers [webpage]. Cancer Research UK (https:\/\/shorturl.at\/SioUv<\/a>).<\/em>
\n 3. Wang H, Guan T, Hu R et al. Targeting KAT7 inhibits the progression of colorectal cancer. Theranostics 2025;15(4):1478\u20131495 (https:\/\/www.thno.org\/v15p1478.htm<\/a>).<\/em><\/p>\n<\/div><\/section>
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