MicroRNA-143 act as a tumor suppressor microRNA in human lung cancer cells by inhibiting cell proliferation, invasion, and migration

Asghariazar, Vahid; Mansoori, Behzad; Kadkhodayi, Mahtab; Safarzadeh, Elham; Mohammadi, Ali; Baradaran, Behzad; Sakhinia, Ebrahim

doi:10.1007/s11033-022-07580-1

Cited by 11 publications

(4 citation statements)

References 47 publications

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“…In a similar manner, the miR-143 downregulation also presented an increased area closure compared to both the control and the respective individual upregulation group at the 24 h and 48 h time points. We need to point out that there have been conflicting reports on miR-143 upregulation, in which it has been stated to either increase or decrease the migration of LC cells [35,[45][46][47][48][49]. However, the miR-143/506 upregulation indicated no appreciable differences in area closure compared to miR-control.…”

Section: Discussionmentioning

confidence: 89%

Stable Dual miR-143 and miR-506 Upregulation Inhibits Proliferation and Cell Cycle Progression

Shrestha,

Lahooti,

Hossian

et al. 2024

IJMS

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The mainstays of lung cancer pathogenesis are cell cycle progression dysregulation, impaired apoptosis, and unregulated cell proliferation. While individual microRNA (miR) targeting or delivering is a promising approach that has been extensively studied, combination of miR targeting can enhance therapeutic efficacy and overcome limitations present in individual miR regulations. We previously reported on the use of a miR-143 and miR-506 combination via transient transfections against lung cancer. In this study, we evaluated the effect of miR-143 and miR-506 under stable deregulations in A549 lung cancer cells. We used lentiviral transductions to either up- or downregulate the two miRs individually or in combination. The cells were sorted and analyzed for miR deregulation via qPCR. We determined the miR deregulations’ effects on the cell cycle, cell proliferation, cancer cell morphology, and cell motility. Compared to the individual miR deregulations, the combined miR upregulation demonstrated a miR-expression-dependent G2 cell cycle arrest and a significant increase in the cell doubling time, whereas the miR-143/506 dual downregulation demonstrated increased cellular motility. Furthermore, the individual miR-143 and miR-506 up- and downregulations exhibited cellular responses lacking an apparent miR-expression-dependent response in the respective analyses. Our work here indicates that, unlike the individual miR upregulations, the combinatorial miR treatment remained advantageous, even under prolonged miR upregulation. Finally, our findings demonstrate potential advantages of miR combinations vs. individual miR treatments.

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Section: Discussionmentioning

confidence: 89%

Stable Dual miR-143 and miR-506 Upregulation Inhibits Proliferation and Cell Cycle Progression

Shrestha,

Lahooti,

Hossian

et al. 2024

IJMS

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“…Our data suggest the miR-143-3p targeting of AKT1 exerts a similar regulatory effect in prostate cancer cells. In relation to other cancers, similar in vitro experiments have consistently shown that miR-143-3p can inhibit proliferation, invasion and migration in different cancer cell lines, including osteosarcoma [ 59 ], ovarian cancer [ 14 ], breast cancer [ 60 ], cervical cancer [ 61 ], laryngeal squamous cell carcinoma [ 62 ], leukaemia [ 63 ] and lung cancer [ 19 ]. Again, these studies all identified different targets through which these effects were mediated.…”

Section: Discussionmentioning

confidence: 99%

“…It is generally considered to act as a tumor suppressor since its expression is downregulated in several cancer types, including ovarian [ 14 ], gastric [ 15 ], breast [ 16 ] and lung [ 17 ] cancer. Additionally, it has been firmly linked with EMT processes in bladder cancer [ 18 , 19 , 20 ], gastric cancer [ 21 ], hepatocellular cancer [ 22 , 23 ], colorectal cancer [ 24 ], breast cancer [ 25 ], oral squamous cell carcinoma [ 26 ], renal cancer [ 27 ] and non-small-cell lung cancer [ 28 ].…”

Section: Introductionmentioning

confidence: 99%

Targeting of AKT1 by miR-143-3p Suppresses Epithelial-to-Mesenchymal Transition in Prostate Cancer

Armstrong,

Willoughby,

McKenna

2023

Cells

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An altered expression of miR-143-3p has been previously reported in prostate cancer where it is purported to play a tumor suppressor role. Evidence from other cancers suggests miR-143-3p acts as an inhibitor of epithelial-to-mesenchymal transition (EMT), a key biological process required for metastasis. However, in prostate cancer the interaction between miR-143-3p and EMT-associated mechanisms remains unclear. Therefore, this paper investigated the link between miR-143-3p and EMT in prostate cancer using in vitro and in silico analyses. PCR detected that miR-143-3p expression was significantly decreased in prostate cancer cell lines compared to normal prostate cells. Bioinformatic analysis of The Cancer Genome Atlas Prostate Adenocarcinoma (TCGA PRAD) data showed a significant downregulation of miR-143-3p in prostate cancer, correlating with pathological markers of advanced disease. Functional enrichment analysis confirmed the significant association of miR-143-3p and its target genes with EMT. The EMT-linked gene AKT1 was subsequently shown to be a novel target of miR-143-3p in prostate cancer cells. The in vitro manipulation of miR-143-3p levels significantly altered the cell proliferation, clonogenicity, migration and expression of EMT-associated markers. Further TCGA PRAD analysis suggested miR-143-3p tumor expression may be a useful predictor of disease recurrence. In summary, this is the first study to report that miR-143-3p overexpression in prostate cancer may inhibit EMT by targeting AKT1. The findings suggest miR-143-3p could be a useful diagnostic and prognostic biomarker for prostate cancer.

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“…A RiboEX reagent was administrated to isolate total RNA (GeneAll, Korea). Using a thermal cycler device, 1 g of total RNA was converted into cDNA (Applied Biosystems, United States) (Asghariazar et al 2022b).…”

Section: Rna Extraction and Qrt-pcrmentioning

confidence: 99%

Sub-chronic exposure to diazinon induce cognitive impairment, alternations in amyloid precursor proteins, and TNF-α expression in the hippocampus of adult rats

Sarailoo

Afshari

Asghariazar

et al. 2023

Preprint

Self Cite

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Organophosphate pesticides such as diazinon (DZN) are involved in the development of psychological symptoms and memory deficits but their effects on the amyloid precursor proteins (APP) genes expression remains unclear. Following low-level oral exposure to the DZN (2 mg/kg), we used novel object recognition, open field, and elevated plus-mazes (EPM) to assess memory and anxiety-like behaviors in rats. We also evaluated alteration in the levels of tumor necrosis factor (TNF-α), amyloid precursor protein (APP), and APP-like protein-2 (APLP2) and real-time quantitative PCR to evaluate the expression of the related genes in the hippocampus. The results showed that DZN exposure increased anxiety-like behaviors, regardless of the duration of exposure, but only extended exposure (12 weeks) impaired memory. The study also found that the hippocampal expression of APP and APLP2 decreased after 12 weeks of exposure, but not after 5 days. The TNF-α gene was up-regulated following 5 days of exposure, but 12 weeks of exposure had no effect. Our finding demonstrates that long-lasting exposure to low levels of DZN in adulthood stimulates APP degradation, which may contribute to poor cognitive outcomes. Given that APP plays a significant role in Alzheimer's disease pathogenesis, alterations in APP expression could contribute to dementia.

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MicroRNA-143 act as a tumor suppressor microRNA in human lung cancer cells by inhibiting cell proliferation, invasion, and migration

Cited by 11 publications

References 47 publications

Stable Dual miR-143 and miR-506 Upregulation Inhibits Proliferation and Cell Cycle Progression

Stable Dual miR-143 and miR-506 Upregulation Inhibits Proliferation and Cell Cycle Progression

Targeting of AKT1 by miR-143-3p Suppresses Epithelial-to-Mesenchymal Transition in Prostate Cancer

Sub-chronic exposure to diazinon induce cognitive impairment, alternations in amyloid precursor proteins, and TNF-α expression in the hippocampus of adult rats

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