MicroRNA-Assisted Hormone Cell Signaling in Colorectal Cancer Resistance

Massaro, Crescenzo; Safadeh, Elham; Sgueglia, Giulia; Stunnenberg, Hendrik G.; Altucci, Lucia; Dell’Aversana, Carmela

doi:10.3390/cells10010039

Cited by 3 publications

(2 citation statements)

References 127 publications

(93 reference statements)

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“… 2019 ; Massaro et al. 2020 ; Wang H 2020 ). Other reports have also demonstrated the importance of STAT signal in regulation of CRC development (Jiang et al.…”

Section: Discussionmentioning

confidence: 99%

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Cardamonin suppressed the migration, invasion, epithelial mesenchymal transition (EMT) and lung metastasis of colorectal cancer cells by down-regulating ADRB2 expression

Zheng

Fan

2022

Pharmaceutical Biology

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Context Cardamonin (CDN) can suppress cell growth in colorectal cancer (CRC), a common digestive malignancy. Objective We explored the effect and mechanism of CDN on metastatic CRC. Materials and methods Two cell lines (HT29 and HCT116) were initially treated with CDN at different concentrations (5, 10 and 20 μmol/L) or 50 μmol/L propranolol (positive control) for 24 or 48 h. Then, the two cell lines were separately transfected with siADRB2 and ADRB2 overexpression plasmids, and further treated with 10 μmol/L CDN for 24 h. The cell viability, migration and invasion were determined by cell counting kit-8 (CCK-8), wound healing and transwell assays, respectively. The levels of ADRB2, matrix metalloprotease (MMP)-2, MMP-9, E-cadherin and N-cadherin were measured by Western blotting or/and RT-qPCR. A CRC metastasis model was established to evaluate the antimetastatic potential of CDN (25 mg/kg). Results ADRB2 (3.2-fold change; p < 0.001) was highly expressed in CRC tissues. CDN at 10 μmol/L suppressed viability (69% and 70%), migration (33% and 66%), invasion (43% and 72%) and ADRB2 expression (2.2- and 2.84-fold change) in HT29 and HCT116 cells ( p < 0.001). CDN at 10 μmol/L inhibited MMP-2, MMP-9 and N-cadherin expression but promoted E-cadherin expression in CRC cells ( p < 0.001). Importantly, the effect of CDN on CRC cells was impaired by ADRB2 overexpression, but further enhanced by ADRB2 down-regulation ( p < 0.01). Additionally, ADRB2 overexpression reversed the inhibitory effect of CDN on metastatic lung nodules ( p < 0.05). Discussion and conclusions: CDN is a potential candidate for the treatment of metastatic CRC in clinical practice.

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“… 2019 ; Massaro et al. 2020 ; Wang H 2020 ). Other reports have also demonstrated the importance of STAT signal in regulation of CRC development (Jiang et al.…”

Section: Discussionmentioning

confidence: 99%

“… 2019 ), breast cancer cells (Massaro et al. 2020 ) and tongue squamous cell carcinoma cells (Liu et al. 2018 ).…”

Section: Discussionmentioning

confidence: 99%

Cardamonin suppressed the migration, invasion, epithelial mesenchymal transition (EMT) and lung metastasis of colorectal cancer cells by down-regulating ADRB2 expression

Zheng

Fan

2022

Pharmaceutical Biology

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The Critical Function of microRNAs in Developing Resistance against 5- Fluorouracil in Cancer Cells

Sheikhnia,

Maghsoudi,

Majidinia

2024

MRMC

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Although there have been significant advancements in cancer treatment, resistance and recurrence in patients make it one of the leading causes of death worldwide. 5-fluorouracil (5-FU), an antimetabolite agent, is widely used in treating a broad range of human malignancies. The cytotoxic effects of 5-FU are mediated by the inhibition of thymidylate synthase (TYMS/TS), resulting in the suppression of essential biosynthetic activity, as well as the misincorporation of its metabolites into RNA and DNA. Despite its huge benefits in cancer therapy, the application of 5-FU in the clinic is restricted due to the occurrence of drug resistance. MicroRNAs (miRNAs) are small, non-coding RNAs that act as negative regulators in many gene expression processes. Research has shown that changes in miRNA play a role in cancer progression and drug resistance. This review examines the role of miRNAs in 5-FU drug resistance in cancers.

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Sex Differences in Colon Cancer: Genomic and Nongenomic Signalling of Oestrogen

Harvey,

Harvey

2023

Genes

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Colon cancer (CRC) is a prevalent malignancy that exhibits distinct differences in incidence, prognosis, and treatment responses between males and females. These disparities have long been attributed to hormonal differences, particularly the influence of oestrogen signalling. This review aims to provide a comprehensive analysis of recent advances in our understanding of the molecular mechanisms underlying sex differences in colon cancer and the protective role of membrane and nuclear oestrogen signalling in CRC development, progression, and therapeutic interventions. We discuss the epidemiological and molecular evidence supporting sex differences in colon cancer, followed by an exploration of the impact of oestrogen in CRC through various genomic and nongenomic signalling pathways involving membrane and nuclear oestrogen receptors. Furthermore, we examine the interplay between oestrogen receptors and other signalling pathways, in particular the Wnt/β-catenin proliferative pathway and hypoxia in shaping biological sex differences and oestrogen protective actions in colon cancer. Lastly, we highlight the potential therapeutic implications of targeting oestrogen signalling in the management of colon cancer and propose future research directions to address the current gaps in our understanding of this complex phenomenon.

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MicroRNA-Assisted Hormone Cell Signaling in Colorectal Cancer Resistance

Cited by 3 publications

References 127 publications

Cardamonin suppressed the migration, invasion, epithelial mesenchymal transition (EMT) and lung metastasis of colorectal cancer cells by down-regulating ADRB2 expression

Cardamonin suppressed the migration, invasion, epithelial mesenchymal transition (EMT) and lung metastasis of colorectal cancer cells by down-regulating ADRB2 expression

The Critical Function of microRNAs in Developing Resistance against 5- Fluorouracil in Cancer Cells

Sex Differences in Colon Cancer: Genomic and Nongenomic Signalling of Oestrogen

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