Knockdown of circ_0055412 promotes cisplatin sensitivity of glioma cells through modulation of CAPG and Wnt/β‐catenin signaling pathway

Zhou, Qina; Fu, Qiang; Mahati, Shaya; Yalikun, Kugeluke; Li, Shaoshan; Dilimulati, Yisireyili

doi:10.1111/cns.13820

Cited by 11 publications

(8 citation statements)

References 39 publications

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“…The role of these proteins in cancer has remained unclear due to conflicting results: while some studies have classified them as oncogenes, others have proposed that they predominantly encompass tumor suppressor functions [ 89 , 90 ]. In addition, only a limited number of studies have investigated the potential role of these proteins in the development of resistance in cancer, particularly in ovarian cancer and gliomas [ 91 , 92 ]. Therefore, it would be necessary to investigate the potential role of all these under-expressed proteins and their various complexes in the development of resistance to anti-HER2 therapies.…”

Section: Discussionmentioning

confidence: 99%

Generation and Characterization of Trastuzumab/Pertuzumab-Resistant HER2-Positive Breast Cancer Cell Lines

Sanz-Álvarez,

Luque,

Morales-Gallego

et al. 2023

IJMS

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The combination of trastuzumab and pertuzumab as first-line therapy in patients with HER2-positive breast cancer has shown significant clinical benefits compared to trastuzumab alone. However, despite initial therapeutic success, most patients eventually progress, and tumors develop acquired resistance and invariably relapse. Therefore, there is an urgent need to improve our understanding of the mechanisms governing resistance in order to develop targeted therapeutic strategies with improved efficacy. We generated four novel HER2-positive cell lines via prolonged exposure to trastuzumab and pertuzumab and determined their resistance rates. Long-term resistance was confirmed by a significant increase in the colony-forming capacity of the derived cells. We authenticated the molecular identity of the new lines via both immunohistochemistry for the clinical phenotype and molecular profiling of point mutations. HER2 overexpression was confirmed in all resistant cell lines, and acquisition of resistance to trastuzumab and pertuzumab did not translate into differences in ER, PR, and HER2 receptor expression. In contrast, changes in the expression and activity of other HER family members, particularly HER4, were observed. In the same vein, analyses of the receptor and effector kinase status of different cellular pathways revealed that the MAPK pathway may be involved in the acquisition of resistance to trastuzumab and pertuzumab. Finally, proteomic analysis confirmed a significant change in the abundance patterns of more than 600 proteins with implications in key biological processes, such as ribosome formation, mitochondrial activity, and metabolism, which could be relevant mechanisms in the generation of resistance in HER2-positive breast cancer. We concluded that these resistant BCCLs may be a valuable tool to better understand the mechanisms of acquisition of resistance to trastuzumab and pertuzumab-based anti-HER2 therapy.

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Section: Discussionmentioning

confidence: 99%

Generation and Characterization of Trastuzumab/Pertuzumab-Resistant HER2-Positive Breast Cancer Cell Lines

Sanz-Álvarez,

Luque,

Morales-Gallego

et al. 2023

IJMS

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“…Increased CAPG expression has been correlated with elevated invasiveness and migration in several human tumor entities like, e.g., glioblastoma [57]. Besides, increased CAPG expression strongly correlates with the resistance to paclitaxel chemotherapy [58], and knockdown of the circular RNA circ_0055412 promotes the cisplatin sensitivity of glioma cells through modulation of the CAPG signaling pathway [59]. Finally, elevated CAPG expression is correlated with unfavorable clinical parameters and poor patients`outcomes in diferent cancers, suggesting a potential role as a biomarker for prognosis and prediction of therapy outcome [60][61][62].…”

Section: Discussionmentioning

confidence: 99%

Tumor Suppressor Role of INPP4B in Chemoresistant Retinoblastoma

Miroschnikov

Dräger

Meenen

et al. 2023

Journal of Oncology

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The chemotherapy of retinoblastoma (RB), a malignant ocular childhood disease, is often limited by the development of resistance against commonly used drugs. We identified inositol polyphosphate 4-phosphatase type II (INPP4B) as a differentially regulated gene in etoposide-resistant RB cell lines, potentially involved in the development of RB resistances. INPP4B is controversially discussed as a tumor suppressor and an oncogenic driver in various cancers, but its role in retinoblastoma in general and chemoresistant RB in particular is yet unknown. In the study presented, we investigated the expression of INPP4B in RB cell lines and patients and analyzed the effect of INPP4B overexpression on etoposide resistant RB cell growth in vitro and in vivo. INPP4B mRNA levels were significantly downregulated in RB cells lines compared to the healthy human retina, with even lower expression levels in etoposide-resistant compared to the sensitive cell lines. Besides, a significant increase in INPP4B expression was observed in chemotherapy-treated RB tumor patient samples compared to untreated tumors. INPP4B overexpression in etoposide-resistant RB cells resulted in a significant reduction in cell viability with reduced growth, proliferation, anchorage-independent growth, and in ovo tumor formation. Caspase-3/7-mediated apoptosis was concomitantly increased, suggesting a tumor suppressive role of INPP4B in chemoresistant RB cells. No changes in AKT signaling were discernible, but p-SGK3 levels increased following INPP4B overexpression, indicating a potential regulation of SGK3 signaling in etoposide-resistant RB cells. RNAseq analysis of INPP4B overexpressing, etoposide-resistant RB cell lines revealed differentially regulated genes involved in cancer progression, mirroring observed in vitro and in vivo effects of INPP4B overexpression and strengthening INPP4B’s importance for cell growth control and tumorigenicity.

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“…As a common upstream regulatory gene of mRNA, miRNA has attracted our attention. Moreover, a quite few miRNA species have been suggested to be biomarkers for glioma 32–34 . For instance, miR‐339/342 can be targeted by FOXD1‐AS1 to regulate glioma biological processes 34 .…”

Section: Discussionmentioning

confidence: 99%

“…Moreover, a quite few miRNA species have been suggested to be biomarkers for glioma. [32][33][34] For instance, miR-339/342 can be targeted by FOXD1-AS1 to regulate glioma biological processes. 34 and Kaposi's Sarcoma.…”

Section: Discussionmentioning

confidence: 99%

LncRNA LINC01018/miR‐942‐5p/KNG1 axis regulates the malignant development of glioma in vitro and in vivo

Wang

Zhao

et al. 2022

CNS Neurosci Ther

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Aims Since the inhibitory effect of KNG1 on glioma has been proved, this study further explores the regulation of the lncRNA/miRNA axis on KNG1 in glioma. Methods The miRNAs that target KNG1 and the lncRNA that targets miR‐942‐5p were predicted by bioinformatics analysis and verified by experiments. The correlations between miR‐942‐5p and the survival of patients and between KNG1 and miR‐942‐5p were analyzed. After transfection, cell migration, invasion, proliferation, and cell cycle were detected through wound healing, Transwell, colony formation, and flow cytometry assays. A mouse subcutaneous xenotransplanted tumor model was established. The expressions of miR‐942‐5p, KNG1, LINC01018, and related genes were evaluated by quantitative real‐time reverse transcription polymerase chain reaction (RT‐qPCR), Western blot, or immunohistochemistry. Results MiR‐942‐5p targeted KNG1, and LINC01018 sponged miR‐942‐5p. The high survival rate of patients was related to low miR‐942‐5p level. MiR‐942‐5p was highly expressed, whereas KNG1 was lowly expressed in glioma. MiR‐942‐5p was negatively correlated with KNG1. Silent LINC01018 or KNG1 and miR‐942‐5p mimic enhanced the migration, invasion, and proliferation of glioma cells, and regulated the expressions of metastasis‐related and proliferation‐related genes. LINC01018 knockdown and miR‐942‐5p mimic promoted glioma tumor growth in mice. The levels of miR‐942‐5p and KNG1 were decreased by LINC01018 knockdown, and LINC01018 expression was suppressed by miR‐942‐5p mimic. MiR‐942‐5p inhibitor, KNG1, and LINC01018 had the opposite effect to miR‐942‐5p mimic. Conclusion LINC01018/miR‐942‐5p/KNG1 pathway regulates the development of glioma cells in vitro and in vivo.

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Knockdown of circ_0055412 promotes cisplatin sensitivity of glioma cells through modulation of CAPG and Wnt/β‐catenin signaling pathway

Cited by 11 publications

References 39 publications

Generation and Characterization of Trastuzumab/Pertuzumab-Resistant HER2-Positive Breast Cancer Cell Lines

Generation and Characterization of Trastuzumab/Pertuzumab-Resistant HER2-Positive Breast Cancer Cell Lines

Tumor Suppressor Role of INPP4B in Chemoresistant Retinoblastoma

LncRNA LINC01018/miR‐942‐5p/KNG1 axis regulates the malignant development of glioma in vitro and in vivo

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