Claudin 3 ELISA Kit (DEIA-XYA425)

Regulatory status: For research use only, not for use in diagnostic procedures.

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Size
96T
Sample
cultured cells
Species Reactivity
Human, Mouse, Rat
Intended Use
The Claudin 3 Cell-Based ELISA Kit is a convenient, lysate-free, high throughput and sensitive assay kit that can monitor Claudin 3 protein expression profile in cells. The kit can be used for measuring the relative amounts of Claudin 3 in cultured cells as well as screening for the effects that various treatments, inhibitors (ie. siRNA or chemicals), or activators have on Claudin 3.
Contents of Kit
1. 96-Well Cell Culture Clear-Bottom Microplate: 1 plate
2. 10x TBS: 24 mL (10x), Clear
3. Quenching Buffer: 24 mL (1x), Clear
4. Blocking Buffer: 50 mL (1x), Clear
5. 10x Wash Buffer: 50 mL (10x), Clear
6. 100x Anti-Claudin 3 Antibody (Rabbit Polyclonal): 60 μL (100x), Purple
7. 100x Anti-GAPDH Antibody (Mouse Monoclonal): 60 μL (100x), Green
8. HRP-Conjugated Anti-Rabbit IgG Antibody: 6 mL (1x), Glass
9. HRP-Conjugated Anti-Mouse IgG Antibody: 6 mL (1x), Glass
10. Primary Antibody Diluent: 12 mL (1x), Clear
11. Ready-to-Use Substrate: 12 mL (1x), Brown
12. Stop Solution: 12 mL (1x), Clear
13. Crystal Violet Solution: 6 mL (1x), Glass
14. SDS Solution: 24 mL (1x), Clear
15. Adhesive Plate Seals: 4 seals
Storage
4°C/6 Months

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References


IPH-926 lobular breast cancer cells are triple-negative but their microarray profile uncovers a luminal subtype

CANCER SCIENCE

Authors: Christgen, Matthias; Geffers, Robert; Kreipe, Hans; Lehmann, Ulrich

Human primary breast cancers and breast cancer cell lines are classified by microarray-defined molecular subtypes, which reflect differentiation characteristics. Estrogen receptor (ER) expression is indicative of the luminal molecular subtype. We have previously established IPH-926, the first well-characterized cell line from infiltrating lobular breast cancer. IPH-926 displays an ER/PR/ErbB2 triple-negative immunophenotype, which is due to a loss of ER expression in its in vivo clonal ancestry. Loss of ER might indicate a fundamental change of cellular differentiation and it is unclear whether a luminal subtype is preserved beyond ER conversion. Using Affymetrix microarray analysis, seven different classifier gene lists (PAM305, DISC256, TN1288, PAM50, UNC1300, LAB704, INT500) and a background population of 50 common mammary carcinoma cell lines, we have now determined the molecular subtype of IPH-926. Strikingly, the IPH-926 expression profile is highly consistent with a luminal subtype. It is nearest to luminal/ER-positive breast cancer cell lines and far apart from basal breast cancer cell lines. Quantitative real-time RT-PCR confirmed enhanced expression of luminal marker genes (AGR2, CLU, CA12, EMP2, CLDN3) and low or absent expression of basal marker genes (KRT5, CD44, CAV1, VIM). Moreover, IPH-926 lacked androgen receptor (AR) expression, a transcription factor previously associated with luminal-like gene expression in a subset of triple-negative or molecular apocrine breast cancers. In conclusion, IPH-926 is triple-negative but belongs to the luminal subtype. Luminal differentiation characteristics can be preserved beyond ER conversion and might not require a compensatory expression of AR.

Bioinformatics analysis of differentially expressed miRNAs in non-small cell lung cancer

JOURNAL OF CLINICAL LABORATORY ANALYSIS

Authors: Yu, Hui; Pang, Zhonghao; Li, Gang; Gu, Tianyi

Objective Non-small cell lung cancer (NSCLC) contains 85% of lung cancer. Lung adenocarcinoma (LUAD) and lung squamous cell carcinoma (LUSC) are the largest NSCLC subgroups. The aim of the study was to investigate the underlying mechanism in developing more effective subtype-specific molecular therapeutic procedures. Methods A total of 876 specimens were used in this study: 494 LUAD tissues (ie, 449 LUAD tissues and 45 matched normal tissues) and 382 LUSC tissues (ie, 337 LUSC tissues and 45 matched normal tissues). The miRNA sequencing data were processed using R. The differential expressed miRNAs between lung cancer and normal tissues were analyzed using the limma package in R. Gene expression, Western blotting, hematoxylin and eosin staining, and luciferase assay were used to test LUAD and LUSC. Results LUAD and LUSC appear sharply distinct at molecular and pathological level. Let-7a-5p, miR-338, miR-375, miR-217, miR-627, miR-140, miR-147b, miR-138-2, miR-584, and miR-197 are top 10 relevant miRNAs and CLDN3, DSG3, KRT17, TMEM125, KRT5, NKX2-1, KRT7, ABCC5, KRAS, and PLCG2 are top 10 relevant genes in NSCLC. At the same time, the miRNAs expression levels were also quite different between the two groups. Among the differential expressed miRNAs, let-7a-5p was significantly down-regulated in LUAD while miR-338 was markedly down-regulated in LUSC. Bioinformatics analyses appeared that let-7a-5p directly targets high-molecular weight keratin 5 (KRT5) which were shown to be a strong risk factor for LUAD. And NK2 homeobox 1(NKX2-1) which was associated with tumor progression in LUSC was identified as a target gene of miR-338. Conclusions Distinct profile of miRNAs can take a part in the development of LUAD and LUSC and thus could serve as a subtype-specific molecular therapeutic target to protect against LUAD and LUSC.

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