Downregulation of nuclear and cytoplasmic Chibby is associated with advanced cervical cancer.

Chibby has been identified as a putative tumor suppressor and antagonist to ß-catenin, thereby controlling the Wnt signaling pathway. Chibby is typically downregulated in numerous types of cancer and may be associated with tumorigenesis. The present study aimed at clarifying the following: i) Whether Chibby antagonizes ß-catenin in cervical cancer; ii) whether Chibby and ß-catenin mRNA expression is associated with cancer progression; and iii) whether Chibby and ß-catenin expression may be used as a biomarker. A total of 87 paraffin-embedded cervical sections with distinct cervical intraepithelial neoplasia (CIN) stages (chronic cervicitis, CIN 1, CIN 2, CIN 3 and invasive squamous cell carcinoma) were collected between June 2004 and October 2012 The mRNA expression level of Chibby and ß-catenin was determined using the polymerase chain reaction. Protein expression and cellular localization of Chibby and ß-catenin were determined using immunohistochemistry. Chibby and ß-catenin were analyzed for possible association with the progression of cervical cancer. Chibby mRNA expression and the Chibby/ß-catenin ratio were identified to be downregulated in invasive tumors. Positive cytoplasmic and nuclear staining for Chibby was associated with CIN staging and decreased as the CIN stage increased. In addition, the cytoplasmic and membrane intensity of ß-catenin was associated with invasive tumors, in which a significantly increased level of protein expression was detected. Chibby may be a tumor suppressor in cervical cancer, since the dysregulation of Chibby expression is associated with tumorigenesis in cervical cancer. Chibby and ß-catenin expression together may potentially to a biomarker for disease progression in cervical cancer.

Molecular Characterization of Community- and Healthcare-Associated Methicillin-Resistant Staphylococcus aureus Isolates in Southern Taiwan.

A growing tendency for community-associated methicillin-resistant Staphylococcus aureus (CA-MRSA) to be involved in nosocomial infections was reported. The predominance of SCCmec type IV or V CA-MRSA in soft tissue infection has also been indicated in Northern Taiwan. To establish basic information about the molecular characteristics of MRSA in our region, a total of 102 MRSA isolates were collected and characterized by an array of typing methods. Healthcare-associated MRSA (HA-MRSA) were found to be more resistant to levofloxacin (p=0.016) and moxifloxacin (p=0.015) than CA-MRSA. However, no difference was found in each and overall SCCmec type distribution between the two MRSA groups. Type I (8.7% vs. 2.6%) was more frequently found in CA-MRSA, whereas type V was more often observed in HA-MRSA (24.4% vs. 8.7%). No difference was found in the dichotomous group of PVL, SCCmec type IV, V, and IV/V between the two MRSA groups. Twenty-seven distinct spa types were identified; t437 and t1081 were the predominant types in our isolates. Moreover, 12 novel spa types with extremely low global frequency were detected in our isolates. SCCmec type III and IV were the major subtypes in the MRSA we collected. The t1081 clones all belonged to HA-MRSA and mostly to SCCmec type V (71.4%). CA-MRSA t437 clones were mostly SCCmec type IV strains (71.4%), but HA-MRSA t437 clones were predominantly SCCmec type IV (42.1%) and III (36.8%). Our findings support a difference in the molecular characteristics of CA-MRSA and HA-MRSA that may reflect various clonal origins in our isolates.

Differential roles of Bcl2L12 and its short variant in breast cancer lymph node metastasis.

Bcl2L12 plays a role in post-mitochondrial apoptosis through multiple mechanisms involving p53, αB-crystallin, caspase-3 and -7 in glioblastoma. Bcl2L12 is reported to be a good prognostic marker in breast cancer and correlated with ER and Bcl2 expression status. However, the mechanisms by which Bcl2L12 regulates apoptosis in breast cancer (BCa) remain unknown. Recent studies have shown that Bcl2L12 expression is a useful biomarker in other types of cancer. Thus, we examined whether Bcl2L12 and Bcl2L12A mRNA were associated with breast cancer progression or a specific subtype. In total, 106 paraffin-embedded, different stage breast cancer specimens were prepared and quantified for Bcl2L12 and Bcl2L12A expression by PCR. The correlation between Bcl2L12 and Bcl2L12A mRNA levels and clinicopathological characteristics was statistically analyzed. The results showed that Bcl2L12 and Bcl2L12A mRNA expression was not significantly different across the different stage, grade and TNM classification groups (P>0.005). Using linear regression, Bcl2L12 mRNA was associated with Bcl2L12A mRNA, grade 3 tumor and the triple-negative breast cancer (TNBC) subtype. In non-TNBC specimens, Bcl2L12 mRNA was only correlated with Bcl2L12A mRNA. Bcl2L12A mRNA was positively associated with Bcl2L12 mRNA and the number of lymph node metastases, but negatively correlated with staging in the non-TNBC group. Specifically, Bcl2L12, but not Bcl2L12A, mRNA was significantly higher in TNBC and grade 3 tumors, respectively. In non-TNBC, Bcl2L12A mRNA was significantly highly expressed in tumors with ≥ 12 metastatic lymph nodes. Bcl2L12 and its variant mRNA were highly expressed in carcinoma in situ (CIS) samples. In addition, they were estimated to be correlated with the total sample and non-TNBC, but not the TNBC group. In summary, a high Bcl2L12 mRNA expression was associated with the high-grade BCa and TNBC subtype. In addition, the interplay between Bcl2L12 and its variant may be associated with high lymph node metastasis in non-TNBC tumors.