Colorectal cancer

Paty, Philip B.; Garcia‐Aguilar, Julio

doi:10.1002/jso.27079

Cited by 10 publications

(6 citation statements)

References 55 publications

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“…In recent decades, considerable advancements in technology and clinical trials have significantly improved the detection, staging, and treatment of CRC. However, despite these developments, CRC remains one of the leading causes of cancer-related deaths worldwide 24 , 25 . One of the significant reasons for its high mortality rate and poor overall survival is late detection 5 .…”

Section: Discussionmentioning

confidence: 99%

Integrated whole transcriptome profiling revealed a convoluted circular RNA-based competing endogenous RNAs regulatory network in colorectal cancer

Mollanoori,

Ghelmani,

Hassani

et al. 2024

Sci Rep

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Recently, it has been identified that circRNAs can act as miRNA sponge to regulate gene expression in various types of cancers, associating them with cancer initiation and progression. The present study aims to identify colorectal cancer-related circRNAs and the underpinning mechanisms of circRNA/miRNA/mRNA networks in the development and progress of Colorectal Cancer. Differentially expressed circRNAs, miRNAs, and mRNAs were identified in GEO microarray datasets using the Limma package of R. The analysis of differentially expressed circRNAs resulted in 23 upregulated and 31 downregulated circRNAs. CeRNAs networks were constructed by intersecting the results of predicted and experimentally validated databases, circbank and miRWalk, and by performing DEMs and DEGs analysis using Cytoscape. Next, functional enrichment analysis was performed for DEGs included in ceRNA networks. Followed by survival analysis, expression profile assessment using TCGA and GEO data, and ROC curve analysis we identified a ceRNA sub-networks that revealed the potential regulatory effect of hsa_circ_0001955 and hsa_circ_0071681 on survival-related genes, namely KLF4, MYC, CCNA2, RACGAP1, and CD44. Overall, we constructed a convoluted regulatory network and outlined its likely mechanisms of action in CRC, which may contribute to the development of more effective approaches for early diagnosis, prognosis, and treatment of CRC.

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Section: Discussionmentioning

confidence: 99%

Integrated whole transcriptome profiling revealed a convoluted circular RNA-based competing endogenous RNAs regulatory network in colorectal cancer

Mollanoori,

Ghelmani,

Hassani

et al. 2024

Sci Rep

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“…Nonmodifiable factors encompass age, race, and genetically predisposing mutations, while modifiable factors encompass aspects such as diet, smoking, and alcohol consumption tendencies, and levels of physical activity 3 . Over the years, advancements in screening and diagnostic methodologies, coupled with the integration of neoadjuvant chemotherapy and radiotherapy protocols prior to surgical interventions, have substantially ameliorated the severity of this ailment 4 …”

Section: Introductionmentioning

confidence: 99%

“…3 Over the years, advancements in screening and diagnostic methodologies, coupled with the integration of neoadjuvant chemotherapy and radiotherapy protocols prior to surgical interventions, have substantially ameliorated the severity of this ailment. 4 CRC manifests as a consequence of specific deficiencies within the DNA repair machinery, critically involving microsatellite instability (MSI) cancers. 5 These MSI cancers arise due to mutations within the mismatch repair system (MMR), primarily implicating a number of proteins, such as MLH1, PMS2, MSH2, and MSH6.…”

Section: Introductionmentioning

confidence: 99%

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Analysis of translesion polymerases in colorectal cancer cells following cetuximab treatment: A network perspective

Das,

Gkoutos,

Acharjee

2024

Cancer Medicine

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IntroductionAdaptive mutagenesis observed in colorectal cancer (CRC) cells upon exposure to EGFR inhibitors contributes to the development of resistance and recurrence. Multiple investigations have indicated a parallel between cancer cells and bacteria in terms of exhibiting adaptive mutagenesis. This phenomenon entails a transient and coordinated escalation of error‐prone translesion synthesis polymerases (TLS polymerases), resulting in mutagenesis of a magnitude sufficient to drive the selection of resistant phenotypes.MethodsIn this study, we conducted a comprehensive pan‐transcriptome analysis of the regulatory framework within CRC cells, with the objective of identifying potential transcriptome modules encompassing certain translesion polymerases and the associated transcription factors (TFs) that govern them. Our sampling strategy involved the collection of transcriptomic data from tumors treated with cetuximab, an EGFR inhibitor, untreated CRC tumors, and colorectal‐derived cell lines, resulting in a diverse dataset. Subsequently, we identified co‐regulated modules using weighted correlation network analysis with a minKMEtostay threshold set at 0.5 to minimize false‐positive module identifications and mapped the modules to STRING annotations. Furthermore, we explored the putative TFs influencing these modules using KBoost, a kernel PCA regression model.ResultsOur analysis did not reveal a distinct transcriptional profile specific to cetuximab treatment. Moreover, we elucidated co‐expression modules housing genes, for example, POLK, POLI, POLQ, REV1, POLN, and POLM. Specifically, POLK, POLI, and POLQ were assigned to the “blue” module, which also encompassed critical DNA damage response enzymes, for example. BRCA1, BRCA2, MSH6, and MSH2. To delineate the transcriptional control of this module, we investigated associated TFs, highlighting the roles of prominent cancer‐associated TFs, such as CENPA, HNF1A, and E2F7.ConclusionWe found that translesion polymerases are co‐regulated with DNA mismatch repair and cell cycle‐associated factors. We did not, however, identified any networks specific to cetuximab treatment indicating that the response to EGFR inhibitors relates to a general stress response mechanism.

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“…Surgery is the primary treatment for patients with nonmetastatic colorectal cancer. However, for patients with locally advanced or metastatic colorectal cancer, chemotherapy is essential[ 2 , 4 ]. Chemotherapy plays an irreplaceable role in the adjuvant therapy of colon cancer and neoadjuvant therapy of rectal cancer.…”

Section: Introductionmentioning

confidence: 99%

Upregulated lncRNA PRNT promotes progression and oxaliplatin resistance of colorectal cancer cells by regulating HIPK2 transcription

Li,

Yang,

Wang

et al. 2024

World J Gastrointest Oncol

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BACKGROUND Colorectal cancer (CRC) is the third most common cancer and a significant cause of cancer-related mortality globally. Resistance to chemotherapy, especially during CRC treatment, leads to reduced effectiveness of drugs and poor patient outcomes. Long noncoding RNAs (lncRNAs) have been implicated in various pathophysiological processes of tumor cells, including chemotherapy resistance, yet the roles of many lncRNAs in CRC remain unclear. AIM To identify and analyze the lncRNAs involved in oxaliplatin resistance in CRC and to understand the underlying molecular mechanisms influencing this resistance. METHODS Gene Expression Omnibus datasets GSE42387 and GSE30011 were reanalyzed to identify lncRNAs and mRNAs associated with oxaliplatin resistance. Various bioinformatics tools were employed to elucidate molecular mechanisms. The expression levels of lncRNAs and mRNAs were assessed via quantitative reverse transcription-polymerase chain reaction. Functional assays, including MTT, wound healing, and Transwell, were conducted to investigate the functional implications of lncRNA alterations. Interactions between lncRNAs and transcription factors were examined using RIP and luciferase reporter assays, while Western blotting was used to confirm downstream pathways. Additionally, a xenograft mouse model was utilized to study the in vivo effects of lncRNAs on chemotherapy resistance. RESULTS LncRNA prion protein testis specific (PRNT) was found to be upregulated in oxaliplatin-resistant CRC cell lines and negatively correlated with homeodomain interacting protein kinase 2 (HIPK2) expression. PRNT was demonstrated to sponge transcription factor zinc finger protein 184 (ZNF184), which in turn could regulate HIPK2 expression. Altered expression of PRNT influenced CRC cell sensitivity to oxaliplatin, with overexpression leading to decreased sensitivity and decreased expression reducing resistance. Both RIP and luciferase reporter assays indicated that ZNF184 and HIPK2 are targets of PRNT. The PRNT/ZNF184/HIPK2 axis was implicated in promoting CRC progression and oxaliplatin resistance both in vitro and in vivo . CONCLUSION The study concludes that PRNT is upregulated in oxaliplatin-resistant CRC cells and modulates the expression of HIPK2 by sponging ZNF184. This regulatory mechanism enhances CRC progression and resistance to oxaliplatin, positioning PRNT as a promising therapeutic target for CRC patients undergoing oxaliplatin-based chemotherapy.

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Colorectal cancer

Cited by 10 publications

References 55 publications

Integrated whole transcriptome profiling revealed a convoluted circular RNA-based competing endogenous RNAs regulatory network in colorectal cancer

Integrated whole transcriptome profiling revealed a convoluted circular RNA-based competing endogenous RNAs regulatory network in colorectal cancer

Analysis of translesion polymerases in colorectal cancer cells following cetuximab treatment: A network perspective

Upregulated lncRNA PRNT promotes progression and oxaliplatin resistance of colorectal cancer cells by regulating HIPK2 transcription

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