scholarly journals Src family kinases, HCK and FGR, associate with local inflammation and tumour progression in colorectal cancer

2019 ◽  
Vol 56 ◽  
pp. 15-22 ◽  
Author(s):  
Antonia K. Roseweir ◽  
Arfon G.M.T. Powell ◽  
Sheryl L. Horstman ◽  
Jitwadee Inthagard ◽  
James H. Park ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Tumour Progression ◽  
Src Family Kinases ◽  
Local Inflammation

scholarly journals PCGF1 promotes epigenetic activation of stemness markers and colorectal cancer stem cell enrichment

2021 ◽  
Vol 12 (7) ◽  
Author(s):  
Guangyu Ji ◽  
Wenjuan Zhou ◽  
Jingyi Du ◽  
Juan Zhou ◽  
Dong Wu ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Stem Cell ◽  
Cancer Progression ◽  
Molecular Mechanisms ◽  
Tumour Progression ◽  
Stem Cell Markers ◽  
Epigenetic Regulator ◽  
Cell Enrichment ◽  
Histone Trimethylation

AbstractColorectal cancer (CRC) stem cells are resistant to cancer therapy and are therefore responsible for tumour progression after conventional therapy fails. However, the molecular mechanisms underlying the maintenance of stemness are poorly understood. In this study, we identified PCGF1 as a crucial epigenetic regulator that sustains the stem cell-like phenotype of CRC. PCGF1 expression was increased in CRC and was significantly correlated with cancer progression and poor prognosis in CRC patients. PCGF1 knockdown inhibited CRC stem cell proliferation and CRC stem cell enrichment. Importantly, PCGF1 silencing impaired tumour growth in vivo. Mechanistically, PCGF1 bound to the promoters of CRC stem cell markers and activated their transcription by increasing the H3K4 histone trimethylation (H3K4me3) marks and decreasing the H3K27 histone trimethylation (H3K27me3) marks on their promoters by increasing expression of the H3K4me3 methyltransferase KMT2A and the H3K27me3 demethylase KDM6A. Our findings suggest that PCGF1 is a potential therapeutic target for CRC treatment.

Soluble serum E-cadherin as a marker of tumour progression in colorectal cancer patients

2004 ◽  
Vol 21 (1) ◽  
pp. 75-78 ◽  
Author(s):  
C. Wilmanns ◽  
J. Grossmann ◽  
S. Steinhauer ◽  
G. Manthey ◽  
B. Weinhold ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cancer Patients ◽  
Tumour Progression ◽  
Colorectal Cancer Patients ◽  
E Cadherin

scholarly journals The Novel Notch-induced Long Noncoding RNA LUNAR1 Determines the Proliferation and Prognosis of Colorectal Cancer

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Zixi Zhang ◽  
Gai Li ◽  
He Qiu ◽  
Jingyi Yang ◽  
Xin Bu ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Noncoding Rna ◽  
Target Genes ◽  
Tumour Progression ◽  
Regulation Of Gene Expression ◽  
Disease Free Survival ◽  
Notch Signalling ◽  
Normal Tissues ◽  
Sw620 Cells ◽  
The Impact

AbstractIn contrast to what is known about the complicated roles of Notch signalling in human malignancies, the direct target genes of Notch signalling are still unclear. Recently, long noncoding RNAs (lncRNAs) have been found to play various roles in the post-transcriptional regulation of gene expression. In the present study, we investigated the potential role of the Notch-induced lncRNA LUNAR1 in colorectal cancer (CRC). We recruited 196 cases of clinical CRC specimens and investigated LUNAR1 levels in these specimens. The associations of LUNAR1 with tumour aggressiveness and clinical outcomes were evaluated. Moreover, the impact of LUNAR1 on the malignant behaviour of tumour cells was tested in cell lines. Significantly increased expression of LUNAR1 in clinical CRC specimens was detected compared with that in matching normal tissues. LUNAR1 expression in CRC was found to be associated with the tumour aggressiveness, disease-free survival and overall survival of patients. The downregulation of LUNAR1 in SW620 cells inhibited cell proliferation, migration, invasion and tumour growth while inducing apoptosis. Moreover, the inhibition of LUNAR1 can significantly suppress IGF1 signalling in CRC. These results indicated that LUNAR1 was increased in CRC and might promote tumour progression. Thus, LUNAR1 may constitute a promising prognostic marker for the clinical management of CRC.

scholarly journals Stereotactic body radiotherapy for bone metastases in patients with colorectal cancer

2020 ◽  
Vol 50 (12) ◽  
pp. 1442-1446
Author(s):  
Kei Ito ◽  
Tatsuro Yamaguchi ◽  
Hiroaki Ogawa ◽  
Yujiro Nakajima ◽  
Katsuyuki Karasawa
Keyword(s):  
Colorectal Cancer ◽  
Bone Metastases ◽  
Stereotactic Body Radiotherapy ◽  
Tumour Progression ◽  
Univariate Analysis ◽  
Target Volume ◽  
Cord Compression ◽  
Local Failure ◽  
Specific Factors ◽  
Poor Outcomes

Abstract Objective To clarify the clinical outcomes of stereotactic body radiotherapy for colorectal cancer-derived bone metastases and identify factors predicting treatment failure. Methods Patients treated with stereotactic body radiotherapy for bone metastases from colorectal cancer between September 2013 and June 2019 were retrospectively reviewed. The prescribed dose for spine and non-spine bone metastases was 24 Gy in two fractions and 35 Gy in five fractions, respectively. The end point was local failure, which was defined as tumour progression on imaging evaluations. In addition, various treatment- and tumour-specific factors were evaluated to determine predictors of local failure. Results This study included 43 lesions in 38 patients, with solitary bone metastases in 18 lesions (42%), re-irradiation stereotactic body radiotherapy in 28 lesions (65%) and postoperative stereotactic body radiotherapy due to spinal cord compression in 10 lesions (23%). The median follow-up after stereotactic body radiotherapy was 12 (range, 2–60) months. The 1-year LF rate was 44%. In the univariate analysis, sacral metastases (P = 0.02) were found to be significantly correlated with LF, and multiple-course systemic therapy before stereotactic body radiotherapy (P= 0.06) and large target volume (P = 0.07) showed a trend towards an association with LF. However, these factors were not independent predictors of LF in the multivariate analysis. Conclusion More than 40% of the lesions treated with stereotactic body radiotherapy for bone metastases from colorectal cancer showed LF within 1 year. No poor prognostic factors could be identified statistically. The poor outcomes in all groups indicate that the treatment intensity of the stereotactic body radiotherapy was insufficient to control colorectal cancer bone metastases.

scholarly journals RNA-binding protein RALY reprogrammes mitochondrial metabolism via mediating miRNA processing in colorectal cancer

Gut ◽  
2020 ◽  
pp. gutjnl-2020-320652
Author(s):  
Lei Sun ◽  
Arabella Wan ◽  
Zhuolong Zhou ◽  
Dongshi Chen ◽  
Heng Liang ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Rna Binding ◽  
Tumour Progression ◽  
Binding Protein ◽  
Rna Binding Protein ◽  
Cancer Therapeutics ◽  
Mitochondrial Metabolism ◽  
The Cancer Genome Atlas ◽  
Colorectal Tumour ◽  
Specific Subset

ObjectiveDysregulated cellular metabolism is a distinct hallmark of human colorectal cancer (CRC). However, metabolic programme rewiring during tumour progression has yet to be fully understood.DesignWe analysed altered gene signatures during colorectal tumour progression, and used a complex of molecular and metabolic assays to study the regulation of metabolism in CRC cell lines, human patient-derived xenograft mouse models and tumour organoid models.ResultsWe identified a novel RNA-binding protein, RALY (also known as hnRNPCL2), that is highly associated with colorectal tumour aggressiveness. RALY acts as a key regulatory component in the Drosha complex, and promotes the post-transcriptional processing of a specific subset of miRNAs (miR-483, miR-676 and miR-877). These miRNAs systematically downregulate the expression of the metabolism-associated genes (ATP5I, ATP5G1, ATP5G3 and CYC1) and thereby reprogramme mitochondrial metabolism in the cancer cell. Analysis of The Cancer Genome Atlas (TCGA) reveals that increased levels of RALY are associated with poor prognosis in the patients with CRC expressing low levels of mitochondrion-associated genes. Mechanistically, induced processing of these miRNAs is facilitated by their N6-methyladenosine switch under reactive oxygen species (ROS) stress. Inhibition of the m6A methylation abolishes the RALY recognition of the terminal loop of the pri-miRNAs. Knockdown of RALY inhibits colorectal tumour growth and progression in vivo and in organoid models.ConclusionsCollectively, our results reveal a critical metabolism-centric role of RALY in tumour progression, which may lead to cancer therapeutics targeting RALY for treating CRC.

scholarly journals Colorectal anastomotic perforation secondary to acute ruptured appendicitis presenting as septic arthritis

2019 ◽  
Vol 5 (2) ◽  
pp. 1
Author(s):  
Hryhoriy Bohdanovych Zhoba ◽  
Brian P. Fleischer ◽  
Wesley B. Vanderlan
Keyword(s):  
Colorectal Cancer ◽  
Septic Arthritis ◽  
Similar Case ◽  
Colonic Perforation ◽  
Anastomotic Leaks ◽  
Local Inflammation ◽  
Rectal Anastomosis ◽  
Common Causes ◽  
Clinically Significant ◽  
Lower Anterior Resection

Anastomotic leaks following abdominoperineal resection with rectal anastomosis become clinically significant in 2.9%-22% of cases. Local recurrence of cancer and local inflammation are the most common causes of these leaks . Colonic perforation presenting with suppurative involvement of the lower extremities has been previously reported. We describe herein the case of a colorectal anastomotic leak secondary to pathology-proved acute appendicitis presenting with suppurative necessitation causing right hip septic arthritis five years following lower anterior resection (LAR) for stage unspecified colorectal cancer. No similar case has been demonstrated in the surveyed literature.

Association of ets-related transcriptional factor E1AF expression with tumour progression and overexpression of MMP-1 and matrilysin in human colorectal cancer

2003 ◽  
Vol 200 (5) ◽  
pp. 568-576 ◽  
Author(s):  
Shina Horiuchi ◽  
Hiroyuki Yamamoto ◽  
Yongfen Min ◽  
Yasushi Adachi ◽  
Fumio Itoh ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Tumour Progression ◽  
Transcriptional Factor ◽  
Human Colorectal Cancer
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