A panel of three plasma microRNAs for colorectal cancer diagnosis

Gastrointestinal cancer (GIC) is a common disease and is considered to be the leading cause of cancer-related death worldwide; thus, new diagnostic and therapeutic strategies for GIC are urgently required. Noncoding RNAs (ncRNAs) are functional RNAs that are transcribed from the genome but do not encode proteins. MicroRNAs (miRNAs) are short ncRNAs that are reported to function as both oncogenes and tumor suppressors. Moreover, several miRNA-based drugs are currently proceeding to clinical trials for various diseases, including cancer. In recent years, the stability of circulating miRNAs in blood has been demonstrated. This is of interest because these miRNAs could be potential noninvasive biomarkers of cancer. In this review, we focus on circulating miRNAs associated with GIC and discuss their potential as novel biomarkers.

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“…The other circulating miRNAs that are reported as biomarkers of CRC are listed in Table 3 [86][87][88][89][90][91][92][93][94].…”

Section: Colorectal Cancermentioning

confidence: 99%

Circulating MicroRNAs in Gastrointestinal Cancer

Ohtsuka

Iwamoto

Naito

et al. 2021

Cancers

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Section: Micrornamentioning

confidence: 99%

“…A total of nine MARKER-related genes are found in CRC, including ATP-binding Cassette Transporter A1 (ABCA1), ATP-binding Cassette Transporter A8 (ABCA8), EGF Containing Fibulin Extracellular Matrix Protein 1 (EFEMP1), Monoamine Oxidase B (MAOB), REarranged during Transfection (RET), StAR Related Lipid Transfer Domain Containing 8 (STARD8), ATP-binding Cassette Transporter A10 (ABCA10), Leucine Rich Repeat Containing 3B (LRRC3B), and Secreted Frizzled Related Protein 1 (SFRP1). Reproduced with permission from Tan et al [ 61 ].…”

Section: Figurementioning

confidence: 99%

“…After all these processes, the mature miRNA is integrated into the RNA inducing silencing complex (RISC) and negatively regulates the expression of several target mRNAs, leading to their degradation or translational inhibition [59,60]. A single miRNA is able to regulate up to hundreds of target mRNAs [61] (Figure 2). In 2002, Calin et al [62] first reported the role of miRNAs in cancer, demonstrating the reduction of miRNA-15 and miRNA-16 in patients with chronic lymphocytic leukemia.…”

Section: Micrornamentioning

confidence: 99%

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Mast Cells, microRNAs and Others: The Role of Translational Research on Colorectal Cancer in the Forthcoming Era of Precision Medicine

Sammarco

Gallo

Vescio

et al. 2020

JCM

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Colorectal cancer (CRC) is a heterogeneous disease, molecularly and anatomically, that develops in a multi-step process requiring the accumulation of several genetic or epigenetic mutations that lead to the gradual transformation of normal mucosa into cancer. In fact, tumorigenesis is extremely complex, with many immunologic and non-immunologic factors present in the tumor microenvironment that can influence tumorigenesis. In the last few years, a role for mast cells (MCs), microRNAs (miRNAs), Kirsten rat sarcoma (KRAS) and v-raf murine sarcoma viral oncogene homologue B (BRAF) in cancer development and progression has been suggested, and numerous efforts have been made to thoroughly assess their correlation with CRC to improve patient survival and quality of life. The identification of easily measurable, non-invasive and cost-effective biomarkers, the so-called “ideal biomarkers”, for CRC screening and treatment remains a high priority. The aim of this review is to discuss the emerging role of mast cells (MCs), microRNAs (miRNAs), KRAS and BRAF as diagnostic and prognostic biomarkers for CRC, evaluating their influence as potential therapy targets in the forthcoming era of precision medicine.

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“…In particular, miR-144-3p inhibited EMT process and cancer metastasis [ 18 – 20 ]. In addition, plasma miR-144-3p level was significantly lower in CRA patients than in healthy controls [ 21 ]. However, the significance of miR-144-3p in CRA remains unclear.…”

Section: Introductionmentioning

confidence: 99%

miR-144-3p inhibited the growth, metastasis and epithelial-mesenchymal transition of colorectal adenocarcinoma by targeting ZEB1/2

Tang

Huang

et al. 2021

Aging

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miR-144-3p is aberrantly expressed in several types of human cancer and functions as a tumor suppressor by inhibiting metastasis. However, the clinical significance and biological function of miR-144-3p in colorectal adenocarcinoma (CRA) have yet to be elucidated. Here we reported that miR-144-3p expression level was significantly down-regulated in CRA tissues compared with matched noncancerous colorectal mucosae tissues. Low miR-144-3p expression was correlated with adverse clinicopathologic characteristics and poor prognosis of CRA patients. Cox regression analysis showed that low miR-144-3p expression was an independent risk factor for DFS and OS in CRA. In vitro and in vivo assays showed that miR-144-3p significantly inhibited proliferation, migration and invasion of CRA cells. In particular, miR-144-3p could suppress EMT process of CRA cells by regulating the cytoskeleton and EMT markers. Bioinformatics analysis indicated that EMT associated transcription factors ZEB1 and ZEB2 were potential targets of miR-144-3p, and miR-144-3p inhibited ZEB1 and ZEB2 expression and was negatively correlated with their expression in CRA. Finally, we confirmed that ZEB1 and ZEB2 down-regulation collaboratively mediated the inhibitory effect of miR-144-3p on proliferation, invasion and EMT of CRA cells. In conclusion, our study provided evidence that miR-144-3p could inhibit CRA cell proliferation, invasion and EMT by targeting ZEB1/2.

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A panel of three plasma microRNAs for colorectal cancer diagnosis

Cited by 37 publications

References 43 publications

Circulating MicroRNAs in Gastrointestinal Cancer

Circulating MicroRNAs in Gastrointestinal Cancer

Mast Cells, microRNAs and Others: The Role of Translational Research on Colorectal Cancer in the Forthcoming Era of Precision Medicine

miR-144-3p inhibited the growth, metastasis and epithelial-mesenchymal transition of colorectal adenocarcinoma by targeting ZEB1/2

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