Identification of a 5-gene-risk score model for predicting luminal A-invasive lobular breast cancer survival

Chen, Yihuan; Zhang, Tao-Feng; Liu, Yiyuan; Zheng, Jiehua; Lin, Weixun; Chen, Yao-Kun; Cai, Jiehui; Zou, Juan; Li, Zhiyang

doi:10.1007/s10709-022-00157-7

Cited by 5 publications

(3 citation statements)

References 59 publications

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“…High levels of the calcium-binding protein 1 (CABP1), as detected after INPP4B overexpression in etoposide-resistant RB355 cells, were likewise revealed by Kaplan–Meier analysis of glioblastoma hub genes and was negatively associated with relapse-free survival of glioblastoma patients [ 68 ]. Besides, CABP1 was identified as one of 5 key prognostic genes for predicting the survival of invasive lobular breast cancer survival [ 69 ]. Additionally, CABP1 can adjust the activity of inositol 1,4,5-triphosphate receptors in a calcium-dependent manner [ 70 ].…”

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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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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“…Another P4-ATPase implicated in breast cancer is ATP8A2. Differential expression analysis with the subsequent univariate Cox regression and LASSO algorithm were used to uncover key prognostic genes for 611 luminal A breast cancer patients [40]. This analysis resulted in a 5-gene-risk score model for predicting luminal A-invasive lobular breast cancer survival.…”

Section: Endometrial Cervical Ovarian and Breast Cancersmentioning

confidence: 99%

“…This analysis resulted in a 5-gene-risk score model for predicting luminal A-invasive lobular breast cancer survival. Specifically, 105 prognostic genes and 9 predictors were identified, allowing the identification of 5-key prognostic genes including ATP8A2 [40]. In another study, analysis of the cells from breast cancer patients demonstrated that no or low expression of ATP11B in conjunction with high expression of PTDSS2, which is negatively regulated by BRCA1, markedly accelerates tumor metastasis and associates with poor prognosis [71].…”

Section: Endometrial Cervical Ovarian and Breast Cancersmentioning

confidence: 99%

Type IV P-Type ATPases: Recent Updates in Cancer Development, Progression, and Treatment

Yazlovitskaya,

Graham

2023

Cancers

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Adaptations of cancer cells for survival are remarkable. One of the most significant properties of cancer cells to prevent the immune system response and resist chemotherapy is the altered lipid metabolism and resulting irregular cell membrane composition. The phospholipid distribution in the plasma membrane of normal animal cells is distinctly asymmetric. Lipid flippases are a family of enzymes regulating membrane asymmetry, and the main class of flippases are type IV P-type ATPases (P4-ATPases). Alteration in the function of flippases results in changes to membrane organization. For some lipids, such as phosphatidylserine, the changes are so drastic that they are considered cancer biomarkers. This review will analyze and discuss recent publications highlighting the role that P4-ATPases play in the development and progression of various cancer types, as well as prospects of targeting P4-ATPases for anti-cancer treatment.

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HPV18 E6/E7 activates Ca²⁺ influx to promote the malignant progression of cervical cancer by inhibiting Ca²⁺ binding protein 1 expression

Kang,

Qiu,

Duo

et al. 2024

Biotech and App Biochem

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Mounting studies have shown that the oncoproteins E6 and E7 encoded by the human papillomavirus (HPV) genome are essential in HPV‐induced cervical cancer (CC). Ca2+ binding protein 1 (CABP1), a downstream target of HPV18‐positive HeLa cells that interferes with E6/E7 expression, was identified through screening the GEO Database (GSE6926). It was confirmed to be down‐regulated in CC through TCGA prediction and in vitro detection. Subsequent in vitro experiments revealed that knocking down E6/E7 inhibited cell proliferation, migration, and invasion, whereas knocking down CABP1 promoted these processes. Simultaneously knocking down CABP1 reversed these effects. Additionally, the results were validated in vivo. Previous studies have indicated that CABP1 can regulate Ca2+ channels, influencing Ca2+ influx and tumor progression. In this study, it was observed that knocking down CABP1 enhanced Ca2+ inflow, as demonstrated by flow cytometry and confocal microscopy. Knocking down E6/E7 inhibited these processes, whereas simultaneously knocking down E6/E7 and CABP1 restored the inhibitory effect of knocking down E6/E7 on Ca2+ inflow. To further elucidate that E6/E7 promotes CC progression by inhibiting CABP1 expression and activating Ca2+ influx, BAPTA/AM treatment was administered during CABP1 knockdown. It was discovered that Ca2+ chelation could reverse the effect of CABP1 knockdown on CC cells. In conclusion, our results offer a novel target for the diagnosis and treatment of HPV‐induced CC.

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Identification of a 5-gene-risk score model for predicting luminal A-invasive lobular breast cancer survival

Cited by 5 publications

References 59 publications

Tumor Suppressor Role of INPP4B in Chemoresistant Retinoblastoma

Tumor Suppressor Role of INPP4B in Chemoresistant Retinoblastoma

Type IV P-Type ATPases: Recent Updates in Cancer Development, Progression, and Treatment

HPV18 E6/E7 activates Ca²⁺ influx to promote the malignant progression of cervical cancer by inhibiting Ca²⁺ binding protein 1 expression

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Identification of a 5-gene-risk score model for predicting luminal A-invasive lobular breast cancer survival

Cited by 5 publications

References 59 publications

Tumor Suppressor Role of INPP4B in Chemoresistant Retinoblastoma

Tumor Suppressor Role of INPP4B in Chemoresistant Retinoblastoma

Type IV P-Type ATPases: Recent Updates in Cancer Development, Progression, and Treatment

HPV18 E6/E7 activates Ca2+ influx to promote the malignant progression of cervical cancer by inhibiting Ca2+ binding protein 1 expression

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HPV18 E6/E7 activates Ca²⁺ influx to promote the malignant progression of cervical cancer by inhibiting Ca²⁺ binding protein 1 expression