scholarly journals A protein complex of SCRIB, NOS1AP and VANGL1 regulates cell polarity and migration, and is associated with breast cancer progression

Oncogene ◽  
2011 ◽  
Vol 31 (32) ◽  
pp. 3696-3708 ◽  
Author(s):  
J N Anastas ◽  
T L Biechele ◽  
M Robitaille ◽  
J Muster ◽  
K H Allison ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Polarity ◽  
Cancer Progression ◽  
Protein Complex ◽  
Breast Cancer Progression ◽  
And Migration

Cell Polarity Proteins in Breast Cancer Progression

2016 ◽  
Vol 117 (10) ◽  
pp. 2215-2223 ◽  
Author(s):  
Carlis Rejon ◽  
Maia Al-Masri ◽  
Luke McCaffrey
Keyword(s):  
Breast Cancer ◽  
Cell Polarity ◽  
Cancer Progression ◽  
Breast Cancer Progression ◽  
Polarity Proteins

scholarly journals Regulatory Mechanisms and Functional Roles of Hypoxia-Induced Long Non-Coding RNA MTORT1 in Breast Cancer Cells

2021 ◽  
Vol 11 ◽  
Author(s):  
Yi-Chun Cheng ◽  
Li-Yu Su ◽  
Li-Han Chen ◽  
Tzu-Pin Lu ◽  
Eric Y. Chuang ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Cancer Progression ◽  
Breast Cancer Cells ◽  
Breast Cancer Progression ◽  
Luciferase Reporter ◽  
Expression Levels ◽  
Endogenous Expression ◽  
And Migration ◽  
Proliferation And Migration

Long non-coding RNAs (lncRNAs) have been found to participate in multiple genetic pathways in cancer. Also, mitochondria-associated lncRNAs have been discovered to modulate mitochondrial function and metabolism. Previously, we identified oxygen-responsive lncRNAs in MCF-7 breast cancer cells under different oxygen concentrations. Among them, a novel mitochondria-encoded lncRNA, mitochondrial oxygen-responsive transcript 1 (MTORT1), was chosen for further investigation. Nuclear, cytoplasmic, and mitochondrial fractionation assays were performed to evaluate the endogenous expression levels of MTORT1 in breast cancer cells. In vitro proliferation and migration assays were conducted to investigate the functions of MTORT1 in breast cancer cells by knockdown of MTORT1. RNA immunoprecipitation and luciferase reporter assays were used to examine the physical binding between MTORT1 and microRNAs. Our results showed that MTORT1 had low endogenous expression levels in breast cancer cells and was mainly located in the mitochondria. Knockdown of MTORT1 enhanced cell proliferation and migration, implying a tumor suppressor role of this novel mitochondrial lncRNA. MTORT1 served as sponge of miR-26a-5p to up-regulate its target genes, CREB1 and STK4. Our findings shed some light on the characterization, function, and regulatory mechanism of the novel hypoxia-induced mitochondrial lncRNA MTORT1, which functions as a microRNA sponge and may inhibit breast cancer progression. These data suggest that MTORT1 may be a candidate for therapeutic targeting of breast cancer progression.

scholarly journals Tripartite motif-containing protein 6 facilitates growth and migration of breast cancer through degradation of STUB1

2021 ◽  
Vol 65 (1) ◽  
Author(s):  
Chuanchao Wei ◽  
Jiayue Wu ◽  
Weiyan Liu ◽  
Jingfeng Lu ◽  
Hongchang Li ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Progression ◽  
Breast Cancer Progression ◽  
Potential Therapeutic Target ◽  
Tripartite Motif ◽  
And Migration ◽  
Breast Cancer Growth

Proteins in the tripartite motif-containing protein (TRIM) family participates in carcinogenesis. However, little attention was focused on the role of TRIM6 on development of breast cancer. Expression level of TRIM6 was found to be markedly enhanced in breast cancer cells and tissues. Functional assays demonstrated that overexpression of TRIM6 promoted breast cancer progression through increase of YAP1 (Yes-associated Protein 1), while knockdown of TRIM6 suppressed in vitro breast cancer progression and in vivo tumor growth through decrease of YAP1. Co-Immunoprecipitation (co-IP) showed that TRIM6 interacted with STUB1 (stress induced phosphoprotein 1 homology and U-box containing protein 1). TRIM6 promoted ubiquitination-mediated degradation of STUB1 to promote YAP1 signaling. Overexpression of STUB1 attenuated TRIM6-induced promotion of breast cancer growth. In conclusion, TRIM6 contributed to breast cancer progression through ubiquitination-dependent proteasomal degradation of STUB1 and provocation of YAP1 pathway, providing potential therapeutic target for breast cancer.

scholarly journals Stage of Breast Cancer Progression Influences Cellular Response to Activation of the WNT/Planar Cell Polarity Pathway

2014 ◽  
Vol 4 (1) ◽  
Author(s):  
Connor D. MacMillan ◽  
Hon S. Leong ◽  
David W. Dales ◽  
Amy E. Robertson ◽  
John D. Lewis ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Polarity ◽  
Cancer Progression ◽  
Cellular Response ◽  
Planar Cell Polarity ◽  
Breast Cancer Progression ◽  
Planar Cell Polarity Pathway

scholarly journals Role of TGF-β receptor III localization in polarity and breast cancer progression

2014 ◽  
Vol 25 (15) ◽  
pp. 2291-2304 ◽  
Author(s):  
Alison E. Meyer ◽  
Catherine E. Gatza ◽  
Tam How ◽  
Mark Starr ◽  
Andrew B. Nixon ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Epithelial Cells ◽  
Cell Surface ◽  
Cell Polarity ◽  
Cancer Progression ◽  
Breast Cancer Progression ◽  
Cell Surface Receptor ◽  
Single Amino Acid ◽  
Migration And Invasion ◽  
Mesenchymal Transition

The majority of breast cancers originate from the highly polarized luminal epithelial cells lining the breast ducts. However, cell polarity is often lost during breast cancer progression. The type III transforming growth factor-β cell surface receptor (TβRIII) functions as a suppressor of breast cancer progression and also regulates the process of epithelial-to-mesenchymal transition (EMT), a consequence of which is the loss of cell polarity. Many cell surface proteins exhibit polarized expression, being targeted specifically to the apical or basolateral domains. Here we demonstrate that TβRIII is basolaterally localized in polarized breast epithelial cells and that disruption of the basolateral targeting of TβRIII through a single amino acid mutation of proline 826 in the cytosolic domain results in global loss of cell polarity through enhanced EMT. In addition, the mistargeting of TβRIII results in enhanced proliferation, migration, and invasion in vitro and enhanced tumor formation and invasion in an in vivo mouse model of breast carcinoma. These results suggest that proper localization of TβRIII is critical for maintenance of epithelial cell polarity and phenotype and expand the mechanisms by which TβRIII prevents breast cancer initiation and progression.

scholarly journals P68 RNA Helicase facilitates Breast Cancer progression by promoting Proliferation and Migration via PDGFR-β/AR axis

2021 ◽  
Vol 12 (21) ◽  
pp. 6543-6552
Author(s):  
Neha Panchbhai ◽  
Chakra R. Turaga ◽  
Malvika Sharma ◽  
Ganesh Satyanarayana ◽  
Zhi-Ren Liu
Keyword(s):  
Breast Cancer ◽  
Cancer Progression ◽  
Rna Helicase ◽  
Breast Cancer Progression ◽  
P68 Rna Helicase ◽  
And Migration ◽  
Proliferation And Migration

scholarly journals MIR22HG inhibits breast cancer progression by stabilizing LATS2 tumor suppressor

2021 ◽  
Vol 12 (9) ◽  
Author(s):  
Xiaochong Deng ◽  
Danrong Ye ◽  
Kaiyao Hua ◽  
Hongming Song ◽  
Qifeng Luo ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Tumor Suppressor ◽  
Cancer Progression ◽  
Noncoding Rna ◽  
Normal Breast ◽  
Breast Cancer Progression ◽  
Large Tumor ◽  
Downstream Target ◽  
And Migration ◽  
Proliferation And Migration

AbstractThe long noncoding RNA called MIR22 host gene (MIR22HG) was previously identified as a tumor suppressor in several cancers. However, the biological function of MIR22HG in breast cancer remains unknown. In this study, we aimed to determine the function and molecular mechanism of MIR22HG in breast cancer progression using transcriptomics and biotechnological techniques. Our results showed that MIR22HG expression was lower in the cancerous tissues than in the paired adjacent normal breast tissues. Additionally, MIR22HG was found to be mainly located in the cytoplasm and acted as a miR-629-5p sponge. Notably, MIR22HG stabilized the expression of large tumor suppressor 2 (LATS2), which promoted the LATS2-dependent phosphorylation of YAP1 and suppressed the expression of its downstream target oncogenes, thereby inhibiting the proliferation and migration of breast cancer cells. Therefore, our findings reveal the MIR22HG-dependent inhibition of breast cancer cell proliferation and migration via the miR-629-5p/LATS2 pathway, providing new insights and identifying novel therapeutic targets for breast cancer treatment.

Beta haemoglobin (hbb) is a novel marker of breast cancer progression

2014 ◽  
Author(s):  
Mattia Capulli ◽  
Adriano Angelucci ◽  
Anna Teti ◽  
Patrizia Sanita ◽  
Luca Ventura ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Progression ◽  
Breast Cancer Progression
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