Crosstalk between long non-coding RNAs and p53 signaling pathway in colorectal cancer: A review study

Mahdi Khanifar, Mohammad; Zafari, Zahra; Sheykhhasan, Mohsen

doi:10.1016/j.prp.2023.154756

Cited by 7 publications

(3 citation statements)

References 164 publications

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“…Each year, colorectal cancer claims the lives of over 900,000 people worldwide, making up 10% of all cancer-related fatalities. The third most frequent cancer is colorectal cancer, and in recent years, its prevalence has been rising(Mahdi Khanifar et al 2023). Although there have been signi cant advancements in traditional cancer treatments, such as robotic surgery, chemotherapeutic medicines, molecular targeted therapeutics, and endoscopic surgery, patients with locally advanced or metastatic colorectal cancer still have poor 5-year overall survival (OS) and disease-free survival (DFS) (Biller et al 2021).…”

Section: Discussionmentioning

confidence: 99%

Galangin cooperates with oxaliplatin to inhibit the proliferation and invasion of colorectal cancer cells by targeting CBX3

Chu,

Lou,

2023

Preprint

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Objective Examining the potential mechanism underlying the effect of galangin combined with oxaliplatin on the invasion and proliferation of colorectal cancer. Methods The effects of galangin combined with oxaliplatin on colorectal cancer (CRC) cell invasion and proliferation were assessed using CCK8 and Transwell assays. Using WB and qPCR, the expression of CBX3 in several CRC cell lines was identified. The levels of CBX3 in normal colorectal tissues and CRC tissues were compared using HPA and GEPIA, and the impact of CBX3 on the prognosis of CRC patients was investigated using GEPIA. To determine whether galangin targets CBX3 to influence the growth and invasion of CRC cells, cell assays were employed. The levels of ROS in HCT116 were measured by immunofluorescence following galangin treatment. The impact of CBX3 on immune cell infiltration in CRC was examined using TIMER. GEPIA produced a list of CBX3-related genes, and R was utilized to perform GO/KEGG enrichment analysis. Results We found that galangin combined with oxaliplatin inhibited the proliferation and invasion of CRC cells and down-regulated the expression of CBX3, which was rescued by overexpression of CBX3. DFS was shorter in those with elevated CBX3 expression. The level of ROS in HCT116 was significantly increased after galangin treatment. The invasion of CD8 + T cells and macrophages in the immunological microenvironment of CRC is favorably linked with increased expression of CBX3. Nuclear chromatin, histone binding, and covalent chromatin modification are enriched regions in CBX3 and related genes. Conclusion Galangin combine with oxaliplatin can inhibit the proliferation and invasion of colorectal cancer cells by down-regulating the expression of CBX3, and CBX3 is highly expressed in colorectal cancer and is related to short DFS.

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Section: Discussionmentioning

confidence: 99%

Galangin cooperates with oxaliplatin to inhibit the proliferation and invasion of colorectal cancer cells by targeting CBX3

Chu,

Lou,

2023

Preprint

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“…Accumulating scientific findings support the pivotal role of lncRNAs in orchestrating various signaling pathways [63][64][65][66][67], offering fresh perspectives for the development of targeted therapies. Presently, DARS-AS1 has been unequivocally established as an important participant in the regulation of multiple cancer-related signaling pathways, as outlined in Figure 5.…”

Section: Signaling Pathways Influenced By Lncrna Dars-as1mentioning

confidence: 99%

DARS-AS1: A Vital Oncogenic LncRNA Regulator with Potential for Cancer Prognosis and Therapy

Shu,

Xia,

Luo

et al. 2024

Int. J. Med. Sci.

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DARS-AS1, short for Aspartyl-tRNA synthetase antisense RNA 1, has emerged as a pivotal player in cancers. Upregulation of this lncRNA is a recurrent phenomenon observed across various cancer types, where it predominantly assumes oncogenic roles, exerting influence on multiple facets of tumor cell biology. This aberrant expression of DARS-AS1 has triggered extensive research investigations, aiming to unravel its roles and clinical values in cancer. In this review, we elucidate the significant correlation between dysregulated DARS-AS1 expression and adverse survival prognoses in cancer patients, drawing from existing literature and pan-cancer analyses from The Cancer Genome Atlas (TCGA). Additionally, we provide comprehensive insights into the diverse functions of DARS-AS1 in various cancers. Our review encompasses the elucidation of the molecular mechanisms, ceRNA networks, functional mediators, and signaling pathways, as well as its involvement in therapy resistance, coupled with the latest advancements in DARS-AS1-related cancer research. These recent updates enrich our comprehensive comprehension of the pivotal role played by DARS-AS1 in cancer, thereby paving the way for future applications of DARS-AS1-targeted strategies in tumor prognosis evaluation and therapeutic interventions. This review furnishes valuable insights to advance the ongoing efforts in combating cancer effectively.

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“…Recent research has shown that even ncRNA plays an important role in this aspect. 8 The interplay between PARP‐1 and BRCA‐1, rescuing defects each other, has been leveraged to develop PARP inhibitors (PARPi) targeting homologous recombination deficient cancers, including CRC. By inhibiting PARP‐1 activity, these inhibitors incapacitate DNA repair mechanisms, leading to the eradication of such cancers.…”

Section: Introductionmentioning

confidence: 99%

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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Crosstalk between long non-coding RNAs and p53 signaling pathway in colorectal cancer: A review study

Cited by 7 publications

References 164 publications

Galangin cooperates with oxaliplatin to inhibit the proliferation and invasion of colorectal cancer cells by targeting CBX3

Galangin cooperates with oxaliplatin to inhibit the proliferation and invasion of colorectal cancer cells by targeting CBX3

DARS-AS1: A Vital Oncogenic LncRNA Regulator with Potential for Cancer Prognosis and Therapy

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

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