Downregulation of miR-155-5p enhances the anti-tumor effect of cetuximab on triple-negative breast cancer cells via inducing cell apoptosis and pyroptosis

Xu, Wen; Song, Chen; Wang, Xiaotong; Li, Yueqi; Bai, Xue; Liang, Xin; Wu, Jingjing; Liu, Jianwen

doi:10.18632/aging.103669

Cited by 42 publications

(32 citation statements)

References 34 publications

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“…The combination of cetuximab with an miR-155-5p antagomir has been demonstrated to enhance the anticancer effects of cetuximab in MDA-MB-468 cells through promoting apoptosis and pyroptosis, both in vitro and in vivo [ 453 ]. Pyroptosis is caspase-1-dependent programmed cell death and is proinflammatory in nature [ 582 ].…”

Section: Combination Strategy For Overcoming Egfri Resistance In Tnbcmentioning

confidence: 99%

“…The common features of this combination effect in vitro and in vivo are the downregulation of p-EGFR and upregulation of gasdermin-E (GSDME). MiR-155-5p directly targets the 3′-UTR of GSDME mRNA [ 453 ]. Of importance, GSDME is a precursor protein of the pore-forming N-terminus of GSDME (GSDME-N) that converts apoptosis to pyroptosis [ 583 , 584 ].…”

Section: Combination Strategy For Overcoming Egfri Resistance In Tnbcmentioning

confidence: 99%

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Potentiating Therapeutic Effects of Epidermal Growth Factor Receptor Inhibition in Triple-Negative Breast Cancer

You

Cho

et al. 2021

Pharmaceuticals

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Triple-negative breast cancer (TNBC) is a subset of breast cancer with aggressive characteristics and few therapeutic options. The lack of an appropriate therapeutic target is a challenging issue in treating TNBC. Although a high level expression of epidermal growth factor receptor (EGFR) has been associated with a poor prognosis among patients with TNBC, targeted anti-EGFR therapies have demonstrated limited efficacy for TNBC treatment in both clinical and preclinical settings. However, with the advantage of a number of clinically approved EGFR inhibitors (EGFRis), combination strategies have been explored as a promising approach to overcome the intrinsic resistance of TNBC to EGFRis. In this review, we analyzed the literature on the combination of EGFRis with other molecularly targeted therapeutics or conventional chemotherapeutics to understand the current knowledge and to provide potential therapeutic options for TNBC treatment.

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Section: Combination Strategy For Overcoming Egfri Resistance In Tnbcmentioning

confidence: 99%

Section: Combination Strategy For Overcoming Egfri Resistance In Tnbcmentioning

confidence: 99%

Potentiating Therapeutic Effects of Epidermal Growth Factor Receptor Inhibition in Triple-Negative Breast Cancer

You

Cho

et al. 2021

Pharmaceuticals

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“…After that, Annexin V-FITC (5 μ L) and PI (10 μ L) were utilized to treat PANC-1 cells in the ark for 15 min. At last, a flow cytometer (BD Biosciences, USA) was utilized to determine apoptotic cells [ 24 ].…”

Section: Methodsmentioning

confidence: 99%

Acidic Tumor Microenvironment Promotes Pancreatic Cancer through miR-451a/MEF2D Axis

Yao

et al. 2022

Journal of Oncology

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Pancreatic cancer (PC), as a highly malignant and aggressive solid tumor, is common in the digestive system. The acidic microenvironment is one of the critical markers of cancer. Nonetheless, there are few studies on how the acidic microenvironment affects the development of PC. This study focused on investigating the specific molecular mechanisms of the acidic microenvironment in PC. In our study, qRT-PCR was conducted for examining microRNA (miR)-451a and myocyte enhancer factor 2D (MEF2D) expressions in PANC-1 cells. Then, detailed functional effects of an acidic environment on miR-451a and MEF2D in PANC-1 cells were detected by CCK-8, colony formation, flow cytometry, wound healing, transwell, mitochondrial functionality measurement, JC-1 staining, DCFH-DA staining, and sphere formation assays. The relationship between miR-451a and MEF2D was confirmed by luciferase reporter analysis. Under acidic conditions, the increase of proliferation, migration, and invasion of PANC-1 cells was observed. Moreover, the mitochondrial oxidative respiration-related gene miR-451a was reduced in acidic conditions. In addition, we found that, in PANC-1 cells under an acidic environment, miR-451a overexpression enhanced oxygen consumption, mitochondrial membrane potential (MMP) loss, and ROS generation and inhibited proliferation, migration, invasion, and stemness via sponging MEF2D. In a word, our results revealed that the acidic microenvironment regulated PC progression by affecting the miR-451a/MEF2D axis, indicating a novel avenue for the future treatment of PC.

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“…It is worth noting that pyroptosis plays a dual role in carcinogenesis and progression [ 19 ]. On one hand, it can inhibit tumor progression by pyroptosis-mediated PCD, and some chemotherapy drugs can exert antitumor functions through inducing pyroptosis [ 19 , 20 ]. On the other hand, the inflammatory cytokines released by pyroptotic cells are conducive to form a suitable microenvironment for tumor cell onset and growth [ 19 , 21 ].…”

Section: Introductionmentioning

confidence: 99%

Pyroptosis regulators exert crucial functions in prognosis, progression and immune microenvironment of pancreatic adenocarcinoma: a bioinformatic and in vitro research

Bai

et al. 2022

Bioengineered

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Pyroptosis is an inflammatory programmed cell death, showing potentials to be a novel anti-cancer approach. However, the roles of pyroptosis-related (PR) genes (PRGs) in pancreatic adenocarcinoma (PAAD) remain elusive. In the present study, we constructed a novel PR risk signature through the lasso regression analysis. The risk signature was greatly conducive to PAAD prognostic assessment. PR risk score was identified as an independent prognostic factor and could distinguish the prognostic differences of most clinical subgroups. Meanwhile, it could improve the traditional prognostic models based on TNM-staging. Next, its prognostic value was also tested in five validation cohorts. Using CIBERSORT, ESTIMATE, and ssGSEA algorithms, the effects of PR risk signature on tumor immune microenvironment (TIM) were explored. High PR risk suppressed antitumor immune through decreasing the infiltrating levels of CD8 T and NK cells. The genomic information and histological expression of risk PRGs were uncovered by USCA and HPA databases. Somatic mutation, methylation alteration, and homozygous CNV of eight PRGs barely occurred in PAAD samples. As for therapeutic correlation, PR risk score may not predict the efficacy of PD-1/L1 inhibitors and was weakly associated with multiple drug susceptibilities. Finally, the biofunctions of toll like receptor 3 (TLR3) in pancreatic cancer (PC) cells were investigated through qPCR, MTT, colony formation, and Transwell assays. Overexpression of TLR3 could promote the proliferation, migration, and invasion of PC cells. In conclusion, PRGs play crucial roles in prognosis, progression, and immune microenvironment of PAAD. TLR3 is expected to be a promising therapeutic target.

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Downregulation of miR-155-5p enhances the anti-tumor effect of cetuximab on triple-negative breast cancer cells via inducing cell apoptosis and pyroptosis

Cited by 42 publications

References 34 publications

Potentiating Therapeutic Effects of Epidermal Growth Factor Receptor Inhibition in Triple-Negative Breast Cancer

Potentiating Therapeutic Effects of Epidermal Growth Factor Receptor Inhibition in Triple-Negative Breast Cancer

Acidic Tumor Microenvironment Promotes Pancreatic Cancer through miR-451a/MEF2D Axis

Pyroptosis regulators exert crucial functions in prognosis, progression and immune microenvironment of pancreatic adenocarcinoma: a bioinformatic and in vitro research

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