Downregulation of miR‑1266‑5P, miR‑185‑5P and miR‑30c‑2 in prostatic cancer tissue and cell lines

Purpose: As a member of the p53 family, p63 is considered to be an important differentiation regulation transcriptional factor, but the roles of p63 in many epithelial tumourigenesis and metastasis processes are still not clear. This study was designed to investigate the expression of p63 and its isoform in normal tissues and squamous cell cancer tissues of uterine cervix, and its significance in cancer cell differentiation. Methods: The expression of p63 was assessed in cervical tissue and cell lines by immunohistochemistry, RT-PCR and Western Blotting. The relationships between p63 protein, various clinico-pathological features, and the differentiation marker involucrin were analyzed. Results: ΔΝp63α is the predominant isoform expressed in cervical epithelial tissues, and it is decreased in moderately or poorly differentiated cervical squamous carcinoma, as well as in the HeLa, SiHa and C33A cervical cancer cell lines. The expression level of ΔΝp63α was positively correlated with that of involucrin in cervical squamous cancer tissue, and the expression of ΔΝp63α is decreased with the degree of tumour invasion. Conclusion: The decrease of ΔΝp63α in cervical squamous cell cancer appears to be associated with the tumour progression, and ΔΝp63α may be a sensitive marker for cervical squamous cancer differentiation.

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A STUDY OF CORRELATIONSHIP BETWEEN THERAPEUTIC EFFICACY OF ANTI-ANDROGEN THERAPY IN PROSTATIC CANCER AND ANDROGEN RECEPTOR CONTENT OF PROSTATIC CANCER TISSUE

The Japanese Journal of Urology ◽

10.5980/jpnjurol1928.75.8_1212 ◽

1984 ◽

Vol 75 (8) ◽

pp. 1212-1224

Author(s):

Kazunori Ohno ◽

Tsugio Umehara ◽

Yoshiaki Kumamoto

Keyword(s):

Androgen Receptor ◽

Therapeutic Efficacy ◽

Prostatic Cancer ◽

Cancer Tissue ◽

Androgen Therapy

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RUNX3 Epigenetic Inactivation Is Associated With Estrogen Receptor Positive Breast Cancer

Journal of Histochemistry & Cytochemistry ◽

10.1369/0022155418797315 ◽

2018 ◽

Vol 66 (10) ◽

pp. 709-721 ◽

Cited By ~ 3

Author(s):

Hui Liu ◽

Zhantao Yan ◽

Qianqian Yin ◽

Kai Cao ◽

Yu Wei ◽

...

Keyword(s):

Breast Cancer ◽

Estrogen Receptor ◽

Cell Lines ◽

Methylation Status ◽

Gene Promoter ◽

Migration And Invasion ◽

Breast Cancer Cell Lines ◽

Cancer Tissue ◽

Er Positive ◽

Runx3 Gene

The role of Runt-related transcription factor 3 ( RUNX3) gene in breast cancer remains not fully understood. We studied the correlation between RUNX3 gene promoter methylation and estrogen receptor (ER) expression status in breast cancer. Three breast cancer cell lines and 113 formalin-fixed, paraffin-embedded breast cancer tissue samples were analyzed for RUNX3 expression. Methylation-specific polymerase chain reaction was used to analyze RUNX3 methylation on the samples. Migration and invasion ability were evaluated in MCF7 cell line (RUNX3 methylated) treated with methylation inhibitor 5-Aza-2′-deoxycytidine (5-Aza-CdR) to study the effect of RUNX3 methylation status. Our data showed that the expression of RUNX3 was high in MCF10A but not in MCF7 and SKBR3 cell lines, while the RUNX3 promoter showed hypermethylation in MCF7 but not in MCF10A and SKBR3. In tissues samples, Immunohistochemical (IHC) expression of RUNX3 protein was higher in ER-negative samples than in ER-positive cases, and it was negatively correlated with the methylation status of the RUNX3 gene promoter. Proliferation, migration, and invasion of MCF7 were suppressed when 5-Aza-CdR treated. Also, the hypermethylation status of RUNX3 gene promoter was reversed and RUNX3 expression was increased. In summary, our data suggest that hypermethylation of the RUNX3 gene promoter may play an important role in ER-positive breast tumor progression.

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Transcriptomic Profiling for the Autophagy Pathway in Colorectal Cancer

International Journal of Molecular Sciences ◽

10.3390/ijms21197101 ◽

2020 ◽

Vol 21 (19) ◽

pp. 7101

Author(s):

Justyna Gil ◽

Paweł Karpiński ◽

Maria M. Sąsiadek

Keyword(s):

Colorectal Cancer ◽

Cell Lines ◽

Enrichment Analysis ◽

Gene Set Enrichment Analysis ◽

Field Cancerization ◽

Cancer Tissue ◽

Mrna Levels ◽

Targeting Therapy ◽

Autophagy Pathway ◽

Using Data

The role of autophagy in colorectal cancer (CRC) pathogenesis appears to be crucial. Autophagy acts both as a tumor suppressor, by removing redundant cellular material, and a tumor-promoting factor, by providing access to components necessary for growth, metabolism, and proliferation. To date, little is known about the expression of genes that play a basal role in the autophagy in CRC. In this study, we aimed to compare the expression levels of 46 genes involved in the autophagy pathway between tumor-adjacent and tumor tissue, employing large RNA sequencing (RNA-seq) and microarray datasets. Additionally, we verified our results using data on 38 CRC cell lines. Gene set enrichment analysis revealed a significant deregulation of autophagy-related gene sets in CRC. The unsupervised clustering of tumors using the mRNA levels of autophagy-related genes revealed the existence of two major clusters: microsatellite instability (MSI)-enriched and -depleted. In cluster 1 (MSI-depleted), ATG9B and LAMP1 genes were the most prominently expressed, whereas cluster 2 (MSI-enriched) was characterized by DRAM1 upregulation. CRC cell lines were also clustered according to MSI-enriched/-depleted subgroups. The moderate deregulation of autophagy-related genes in cancer tissue, as compared to adjacent tissue, suggests a prominent field cancerization or early disruption of autophagy. Genes differentiating these clusters are promising candidates for CRC targeting therapy worthy of further investigation.

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Hypoxia and expression of the proapoptotic regulator BNIP3 in cervical cancer

International Journal of Gynecological Cancer ◽

10.1136/ijgc-00009577-200605000-00055 ◽

2006 ◽

Vol 16 (3) ◽

pp. 1314-1320 ◽

Cited By ~ 4

Author(s):

C. Leo ◽

L. C. Horn ◽

M. HÖCKEL

Keyword(s):

Cervical Cancer ◽

Cell Lines ◽

Cancer Cell ◽

Northern Blot ◽

Blot Analysis ◽

Northern Blot Analysis ◽

Cancer Cell Lines ◽

Cervical Cancer Cell ◽

Clinical Samples ◽

Cancer Tissue

Hypoxia plays a major role in the malignant progression of tumors. Here, we investigate the expression of Bcl-2/adenovirus E1B 19 kd-interacting protein 3 (BNIP3), a proapoptotic Bcl-2 family member, and its relationship to hypoxia in cervical cancer cell lines and clinical samples of cervical cancer. Cervical cancer cell lines were grown under hypoxia or normoxia, and BNIP3 mRNA expression was examined by Northern blot analysis. In 50 patients with cervical cancer, intratumoral oxygen measurement with the Eppendorf electrode and needle biopsies of the tumor were performed. The obtained tissue was subsequently analyzed by immunohistochemistry with an anti-BNIP3 antibody. Cervical cancer tissue collected upon surgery was used for Northern blot analysis of in vivo BNIP3 mRNA expression. BNIP3 mRNA is strongly induced under hypoxic conditions in all cervical cancer cell lines investigated. Furthermore, Northern blot analysis revealed that BNIP3 mRNA is expressed in cervical cancer tissue. Using immunohistochemistry, we demonstrated that BNIP3 protein is expressed in 82% of the investigated cervical cancers and that more advanced tumor stages showed significantly stronger BNIP3 expression. However, we observed no correlation between BNIP3 expression and intratumoral hypoxia. In conclusion, BNIP3 is expressed in different cervical cancer cell lines as well as in clinical samples of cervical cancer. Although BNIP3 is clearly hypoxia-inducible in vitro, our results suggest additional mechanisms of BNIP3 regulation in vivo. Our findings therefore highlight a discrepancy between in vitro models of tumor hypoxia and the complexity of human cancer.

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