Molecular Regulation of Cancer Cell Migration, Invasion, and Metastasis

Tahtamouni, Lubna H.; Ahram, Mamoun; Koblinski, Jennifer E.; Rolfo, Christian

doi:10.1155/2019/1356508

Cited by 52 publications

(39 citation statements)

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“…Epithelial OC patients receiving chemotherapy usually develop acquired drug resistance within one year, which leads to tumor recurrence and uncontrolled metastases [ 65 ]. Metastasis, one of the most important hallmarks of malignancy, is a complex process that involves migration and invasion of cancer cells [ 66 , 67 , 68 ]. Several studies have suggested that chemotherapy resistance is acquired by the metastatic growth of tumor cells that may closely parallel each other [ 69 , 70 , 71 ].…”

Section: Discussionmentioning

confidence: 99%

Establishment of Acquired Cisplatin Resistance in Ovarian Cancer Cell Lines Characterized by Enriched Metastatic Properties with Increased Twist Expression

Bahar

Kim

et al. 2020

IJMS

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Ovarian cancer (OC) is the most lethal of the gynecologic cancers, and platinum-based treatment is a part of the standard first-line chemotherapy regimen. However, rapid development of acquired cisplatin resistance remains the main cause of treatment failure, and the underlying mechanism of resistance in OC treatment remains poorly understood. Faced with this problem, our aim in this study was to generate cisplatin-resistant (CisR) OC cell models in vitro and investigate the role of epithelial–mesenchymal transition (EMT) transcription factor Twist on acquired cisplatin resistance in OC cell models. To achieve this aim, OC cell lines OV-90 and SKOV-3 were exposed to cisplatin using pulse dosing and stepwise dose escalation methods for a duration of eight months, and a total of four CisR sublines were generated, two for each cell line. The acquired cisplatin resistance was confirmed by determination of 50% inhibitory concentration (IC50) and clonogenic survival assay. Furthermore, the CisR cells were studied to assess their respective characteristics of metastasis, EMT phenotype, DNA repair and endoplasmic reticulum stress-mediated cell death. We found the IC50 of CisR cells to cisplatin was 3–5 times higher than parental cells. The expression of Twist and metastatic ability of CisR cells were significantly greater than those of sensitive cells. The CisR cells displayed an EMT phenotype with decreased epithelial cell marker E-cadherin and increased mesenchymal proteins N-cadherin and vimentin. We observed that CisR cells showed significantly higher expression of DNA repair proteins, X-ray repair cross-complementing protein 1 (XRCC1) and poly (ADP-ribose) polymerases 1 (PARP1), with significantly reduced endoplasmic reticulum (ER) stress-mediated cell death. Moreover, Twist knockdown reduced metastatic ability of CisR cells by suppressing EMT, DNA repair and inducing ER stress-induced cell death. In conclusion, we highlighted the utilization of an acquired cisplatin resistance model to identify the potential role of Twist as a therapeutic target to reverse acquired cisplatin resistance in OC.

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Section: Discussionmentioning

confidence: 99%

Establishment of Acquired Cisplatin Resistance in Ovarian Cancer Cell Lines Characterized by Enriched Metastatic Properties with Increased Twist Expression

Bahar

Kim

et al. 2020

IJMS

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“…Metastasis is a multi-step process that involves the migration and invasion of cancer cells and is a sign of malignancy [37]. Inhibition of migration of cells treated with E. purpura's extract can indicate the anticancer properties of Echinacea.…”

Section: Discussionmentioning

confidence: 99%

Effect of Echinacea purpura’s extract on the expression of VEGF-A gene and antiproliferative, induction of apoptosis, inhibition of cell migration, and colony formation on gastric cancer cell line AGS

Moradian

Sadeghi

Sabouni³

et al. 2020

Preprint

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Background Echinacea purpura extract, one of the main compounds of which is caffeic acid, has anti-cancer and anti-angiogenic properties. In the present study, the anticancer effect of E. purpur’s extract was investigated on the growth of gastric cancer cell line AGS, induction of apoptosis and inhibition of cell migration, and colony formation as well as the expression level of VEGF-A gene. Methods E. purpura’s extract was extracted using Soxhlet device and HPLC chromatography was used to confirm the presence of caffeic acid in the extract. Cell proliferation was detected using MTT and colony formation assay. In vitro invasion of cancer cells was measured using scratch assay. Apoptosis assay was performed using AO/EB double staining. The anti-angiogenesis effect of the extract was an investigation of VEGF-A gene expression after treatment with the extracts using Real-time PCR. Results The result showed that the cell viability percentage after-treatment of the plant extract in a concentration of 2.0, 2.75 and 3.25 mg/ml and standard caffeic acid in a concentration of 600, 750 and 850 mM were 80, 50 and 26% as well as 81, 49, and 27%, respectively. In AGS cells treated with the concentration of 2, 2.75, and 3.25 mg/ml, dose-dependent the orange-red fluorescence was increased and indicating the emergence of apoptosis. The assessment of the wound healing area showed no significant differences between 24 and 48 h compared to 0 h in the treatment groups (P>0.05). E.purpura’s extract supressed the formation of colonies in AGS cancer cells in a dose dependent manner. The expression level of the VEGF-A gene at a concentration of 2.0, 2.75 and 3.25 mg/ml the plant extract reduced by 0.9, 0.87 and 0.85 fold, respectively. Conclusion E. purpura’s extract could effectively inhibit AGS gastric cancer cell proliferation, migration, colony formation, and reduce VEGF-A expression and induce apoptosis.

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“…Neoplastic metastasis typifies an advanced phase of malignancy, thus, resulting in fatality in around 90% of cancer cases [ 56 , 86 ]. Metastasis is known to be a multiphase mechanism that involves invasion and migration of the tumor cells to neighboring tissues or organs [ 35 ].…”

Section: Anticancer Attributes Of Ctdmentioning

confidence: 99%

Anticancer Attributes of Cantharidin: Involved Molecular Mechanisms and Pathways

Naz

Zhang

et al. 2020

Molecules

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Cancer is a preeminent threat to the human race, causing millions of deaths each year on the Earth. Traditionally, natural compounds are deemed promising agents for cancer treatment. Cantharidin (CTD)—a terpenoid isolated from blister beetles—has been used extensively in traditional Chinese medicines for healing various maladies and cancer. CTD has been proven to be protein phosphatase 2A (PP2A) and heat shock transcription factor 1 (HSF-1) inhibitor, which can be potential targets for its anticancer activity. Albeit, it harbors some toxicities, its immense anticancer potential cannot be overlooked, as the cancer-specific delivery of CTD could help to rescue its lethal effects. Furthermore, several derivatives have been designed to weaken its toxicity. In light of extensive research, the antitumor activity of CTD is evident in both in vitro as well as in vivo cancer models. CTD has also proven efficacious in combination with chemotherapy and radiotherapy and it can also target some drug-resistant cancer cells. This mini-review endeavors to interpret and summarize recent information about CTD anticancer potential and underlying molecular mechanisms. The pertinent anticancer strength of CTD could be employed to develop an effective anticarcinogenic drug.

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Molecular Regulation of Cancer Cell Migration, Invasion, and Metastasis

Cited by 52 publications

References 0 publications

Establishment of Acquired Cisplatin Resistance in Ovarian Cancer Cell Lines Characterized by Enriched Metastatic Properties with Increased Twist Expression

Establishment of Acquired Cisplatin Resistance in Ovarian Cancer Cell Lines Characterized by Enriched Metastatic Properties with Increased Twist Expression

Effect of Echinacea purpura’s extract on the expression of VEGF-A gene and antiproliferative, induction of apoptosis, inhibition of cell migration, and colony formation on gastric cancer cell line AGS

Anticancer Attributes of Cantharidin: Involved Molecular Mechanisms and Pathways

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