Studies on selected molecular factors in endometrial cancers

Markowska, Anna; Szarszewska, Monika; Żurawski, Jakub; Sajdak, Stefan; Knapp, Paweł; Gryboś, Anna; Olejek, Anita; Bednarek, Wiesława; Roszak, A.; Jóźwik, Marcin; Marszałek, Andrzej; Filas, Violetta; Wójcik‐Krowiranda, Katarzyna; Mądry, Radosław; Markowska, Janina; Sozański, Rafał

doi:10.17219/acem/70861

Cited by 4 publications

(5 citation statements)

References 32 publications

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“…Endometrial cancer is one of the most common malignant tumors of females (Szarszewska et al, 2019). It is a malignant tumor that occurs in the epithelial tissues of postmenopausal women (Smith et al, 2017).…”

Section: Introductionmentioning

confidence: 99%

miR-379-5p inhibits proliferation and invasion of the endometrial cancer cells by inhibiting expression of ROR1

Mao¹,

Chen²,

Min³

2021

Acta Biochim Pol

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Endometrial cancer is a common gynecological malignancy, and the incidence of this disease has increased in recent years. Recently, some studies suggested that the expression of miR-379-5p suppressed the metastasis of breast cancer cells. However, whether the expression of miR-379-5p could affect the proliferation, migration and invasion of endometrial cancer is unclear. In this study, we established miR-379-5p overexpression and miR-379-5p inhibition in endometrial cancer cells. Next, EdU and colony formation assays were performed to measure proliferation of endometrial cancer cells. Wound healing and transwell assays were carried out to examine the migration and invasion of these cells. Then, luciferase reporter assay was performed to test the relationship between miR-379-5p and ROR1. Finally, we overexpressed ROR1 in miR-379-5p overexpressing endometrial cancer cells. Colony formation, wound healing and transwell assays were used to measure proliferation, migration and invasion of these cells. The results showed that overexpression of miR-379-5p repressed proliferation, migration and invasion of endometrial cancer cells. Higher levels of miR-379-5p repressed expression of N-cadherin, Vimentin and ZEB1. Overexpression of miR-379-5p also promoted expression of E-cadherin and ZO-1. In addition, miR-379-5p targeted and suppressed expression of ROR1. Overexpression of ROR1 abolished the inhibitory effect of miR-379-5p on proliferation, migration, invasion and EMT of endometrial cancer cells. All of these results indicated that miR-379-5p suppressed proliferation, migration and invasion of endometrial cancer cells by inhibiting the expression of ROR1 and the EMT process.

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Section: Introductionmentioning

confidence: 99%

miR-379-5p inhibits proliferation and invasion of the endometrial cancer cells by inhibiting expression of ROR1

Mao¹,

Chen²,

Min³

2021

Acta Biochim Pol

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“…However, other studies have suggested that the expression of ERβ is upregulated in higher cancer stages. However, these authors differentiated the patients into two groups: patients exhibiting the IA FIGO stage and others exhibiting higher stages of EC; this narrows the interpretation of the results [23].…”

Section: Discussionmentioning

confidence: 95%

“…It upregulates the proliferation, migration, and angiogenesis of cells, and inhibits their apoptosis [16]. In early-stage EC, higher ERα expression has been observed [23].…”

Section: Discussionmentioning

confidence: 99%

Estrogen Receptor (ER) and Progesterone Receptor (PgR) Expression in Endometrial Cancer—An Immunohistochemical Assessment

Przewoźny,

Rogaliński,

de Mezer

et al. 2024

Diagnostics

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Endometrial cancer (EC) is one of the most common types of cancer in Poland and worldwide. Many risk factors lead to the pathogenesis of this disease, such as lifestyle choices, BMI, the medicines used in breast cancer therapy, and Lynch syndrome. EC cells show the expression of estrogen receptors (ERs) and progesterone receptors (PgR). These receptors occur in multiple isoforms and have a significant influence on the operation of cells. The loss of ER and PgR expression is associated with a poor prognosis. We assessed tissue slides that were obtained from 103 women with EC diagnoses of various grades, stages, and histological types. In this study, we used computer image analyses to increase the objectivity of the assessment. We proved that, in the tissue of patients with high-grade (G3) EC, the expression of PgR is significantly lower than that in the tissues of patients with low-grade EC. We also observed that PgR is significantly expressed in EC with a low FIGO stage and in the endometroid type of EC (which rarely becomes malignant compared to serous type). The expression of ERb1 was lower in patients with EC at the IV FIGO stage than in patients with stage III EC. These findings confirm that the loss of ER and PgR expression is connected with a poor prognosis.

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“…The HGF/cMet signaling pathway is hyperactive in various solid tumors, including EC (12,31). The level of HGF significantly increased in patients with endometriosis (32), indicating that the HGF/cMet pathway might be vital in endometrial diseases.…”

Section: Discussionmentioning

confidence: 99%

Dual inhibition of RNAi therapeutic miR-26a-5p targeting cMet and immunotherapy against EGFR in endometrial cancer treatment

Liu¹,

Cai²,

Chang³

2021

Ann Transl Med

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Background: Precise prediction of drug combination targeting tumor cells effectively is a crucial challenge for tumor therapy, especially for endometrial cancer (EC). Considering the resistance, crosstalk that occurs between the receptor tyrosine kinase mesenchymal-epithelial transition factor (cMet) and epidermal growth factor receptor (EGFR), and their indispensable influence on the occurrence of EC, this study aimed to explore a novel therapeutic approach for EC treatment through blocking cMet and EGFR simultaneously.Methods: In the present study, the expression of miR-26a-5p in EC cell lines was detected using quantitative real-time polymerase chain reaction assay. The potential role of miR-26a-5p in the development of EC was examined using cell counting kit assay, 5-ethynyl-2'-deoxyuridine staining, wound healing assay, and cell apoptosis staining assay. Subsequently, the effect of upregulated miR-26a-5p in vivo was confirmed on a xenograft model. Luciferase reporter assay and Western blot analysis were performed to verify the relation between miR-26a-5p and cMet. Furthermore, the dual therapeutic effect of miR-26a-5p and EGFR monoclonal antibody cetuximab was confirmed in vivo and in vitro. Results:The results indicated that miR-26a-5p expression significantly reduced in EC cell lines compared with the normal endometrial cell line. Furthermore, the overexpression of miR-26a-5p inhibited the progression of EC, including cell migration, cell proliferation, and cell apoptosis in vivo and in vitro.Subsequently, mir-26a-5p regulated the expression of cMet and the downstream the hepatocyte growth factor (HGF)/cMet pathway, thus exerting an inhibitory effect on EC cells. In addition, the study also demonstrated that the upregulation of miR-26a-5p could significantly enhance the inhibitory effect of cetuximab compared with the use of cetuximab alone in vivo and in vitro.Conclusions: RNAi therapeutic miR-26a-5p suppressed the progression of EC through regulating the cMet/HGF pathway. The dual therapy using RNA interference and neutralizing antibody simultaneously blocked tumor targets, including cMet and EGFR, thus providing a novel approach for overcoming the resistance to the inhibitors against a single target in EC treatment.

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Studies on selected molecular factors in endometrial cancers

Cited by 4 publications

References 32 publications

miR-379-5p inhibits proliferation and invasion of the endometrial cancer cells by inhibiting expression of ROR1

miR-379-5p inhibits proliferation and invasion of the endometrial cancer cells by inhibiting expression of ROR1

Estrogen Receptor (ER) and Progesterone Receptor (PgR) Expression in Endometrial Cancer—An Immunohistochemical Assessment

Dual inhibition of RNAi therapeutic miR-26a-5p targeting cMet and immunotherapy against EGFR in endometrial cancer treatment

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