Triple-Negative or Close-to-Triple-Negative Breast Cancer Presenting as a Thick-Walled Cystic Lesion.

Clinical and pathologic characteristics of the invasive ductal carcinoma (IDC) presenting as a thick-walled breast cyst are little known. Three female patients were included in this report. A palpable, nontender breast lump was found in all cases. While mammography showed a hyperdense mass, ultrasonography demonstrated a thick-walled cystic mass. Magnetic resonance imaging clearly showed the cystic breast lesions with ring-like or irregular rim enhancement. A grade III IDC was confirmed in all cases. All IDCs but one were estrogen receptor negative, progesterone receptor negative, and human epidermal growth factor receptor 2 negative, with merely weak progesterone receptor positivity (5%) in one case. All cases underwent surgical management first and postoperative chemotherapy. Breast malignancy presenting as a thick-walled cystic mass could be a highly aggressive IDC, even triple-negative breast cancer. It is imperative for breast cancer-related practitioners to identify the potentially malignant cystic lesions timely and adopt appropriate management.

Comparison of splinting immobilization and K-wire fixation in children with type II phalange neck fracture.

To compare outcomes of type II phalangeal neck fractures in children who received closed reduction followed by splinting immobilization or by K-wire fixation. Furthermore, we analyzed the remodeling potential of residual deformities and the relationship between age and outcomes. Patients in Children's Hospital of Fudan University, Xiamen Hospital were included in the study from October 2015 to October 2018. We compared outcomes between the conservation group and operation group. Remodeling of residual deformities was calculated on a series of anteroposterior and lateral radiography. The correlation between age and outcomes was analyzed using Spearman's rank correlation coefficient. Forty patients (25 males) were enrolled. Nineteen patients had subtype IIa, 19 subtype IIb, and two subtype IIc fractures. Left hands were affected more than right hands, and small finger and proximal phalanx were more frequently involved. There were no significant differences between conservation group and operation group among excellent, good, and fair outcomes. And the outcomes were not significantly different between the IIa and IIb subtypes. An average sagittal remodeling rate was 88.5%, and coronal remodeling rate was 56.71%, respectively, in 13 patients with residual deformities. There was a significant correlation between age and final outcomes. Closed reduction and stable splint fixation may be an effective and economical initial treatment option. Fracture subtype does not seem to be a key factor for choosing treatment options. The fractured phalangeal neck had remodeling potential whether on sagittal or coronal plane. Younger age might be a predictor of better outcomes in children with type II phalanx neck fractures.

Emerging roles of interactions between ncRNAs and other epigenetic modifications in breast cancer.

Up till the present moment, breast cancer is still the leading cause of cancer-related death in women worldwide. Although the treatment methods and protocols for breast cancer are constantly improving, the long-term prognosis of patients is still not optimistic due to the complex heterogeneity of the disease, multi-organ metastasis, chemotherapy and radiotherapy resistance. As a newly discovered class of non-coding RNAs, ncRNAs play an important role in various cancers. Especially in breast cancer, lncRNAs have received extensive attention and have been confirmed to regulate cancer progression through a variety of pathways. Meanwhile, the study of epigenetic modification, including DNA methylation, RNA methylation and histone modification, has developed rapidly in recent years, which has greatly promoted the attention to the important role of non-coding RNAs in breast cancer. In this review, we carefully and comprehensively describe the interactions between several major classes of epigenetic modifications and ncRNAs, as well as their different subsequent biological effects, and discuss their potential for practical clinical applications.

Predictors of residual hip dysplasia in 12-18-month-old vs. over 18-month-old DDH patients after closed reduction and the reliability of one residual hip dysplasia criterion: a retrospective cohort study.

Background: The diagnostic and prediction criteria of residual hip dysplasia (RHD) remains controversial. There were no studies that focused on the risk factors of RHD after closed reduction (CR) in children with developmental dislocation of the hips (DDH) over 12 months of age. In this study, we assessed the percentage of RHD in DDH patients aged 12 to 18 months vs. that in DDH patients aged over 18 months after CR and determine the predictors of RHD. Meanwhile, we tested the reliability of our RHD criteria compared with Harcke standard. Methods: Patients over 12 months of age who underwent successful CR from October 2011 to November 2017 and followed up for at least 2 years were enrolled. Gender, affected side, age at CR and follow-up time were recorded. Acetabular index (AI), horizontal acetabular width (AWh), center-to-edge angle (CEA), and femoral head coverage (FHC) were measured. The cases were divided into two groups according to whether older than 18 months. RHD was determined according to our criteria. Results: A total of 82 patients (107 hips) were included, including 69 females (84.1%), 13 males (15.9%), 25 patients (30.5%) with bilateral DDH, 33 patients (40.2%) with left side, 24 patients (29.3%) with right side, 40 patients (49 hips) with age 12-18 months, and 42 patients (58 hips) with age >18 months. At a mean follow-up of 47.8 [24-92] months, the percentage of RHD was higher in patients >18 months of age (58.6%) than patients 12-18 months of age (40.8%), but the difference was not statistically significant. Binary logistic regression analysis showed that pre-AI, pre-AWh, and improvement in AI and AWh (P=0.025, 0.016, 0.001, 0.003, respectively) had significant difference. The sensitivity and specialty of our RHD criteria were 81.82% and 82.69%, respectively. Conclusions: For patients with DDH over 18 months, CR is still a choice. We documented four predictors of RHD, suggesting that we should focus on the developmental potential of an individual's acetabulum. Our RHD criteria may be one of the reliable and useful tools in clinical practice to help determine whether to perform continuous observation or surgery, but further research is needed due to limited sample size and follow-up time.

LncRNA IPW inhibits growth of ductal carcinoma in situ by downregulating ID2 through miR-29c.

BACKGROUND: Ductal carcinoma in situ (DCIS) of breast is the noninvasive lesion that has propensity to progress to the malignant form. At present, it is still unknown which lesions can potentially progress to invasive forms. In this study, we aimed to identify key lncRNAs involved in DCIS growth. METHODS: We employ disease-related lncProfiler array to identify IPW in specimens of DCIS and matching control samples and validate the observations in three DCIS-non-tumorigenic cell lines. Further, we examine the mechanism of IPW action and the downstream signaling in in vitro and in vivo assays. Importantly, we screened a library containing 390 natural compounds to identify candidate compound selectively inhibiting IPW low DCIS cells. RESULTS: We identified lncRNA IPW as a novel tumor suppressor critical for inhibiting DCIS growth. Ectopic expression of IPW in DCIS cells strongly inhibited cell proliferation, colony formation and cell cycle progression while silencing IPW in primary breast cells promoted their growth. Additionally, orthotropic implantation of cells with ectopic expression of IPW exhibited decreased tumor growth in vivo. Mechanistically, IPW epigenetically enhanced miR-29c expression by promoting H3K4me3 enrichment in its promoter region. Furthermore, we identified that miR-29c negatively regulated a stemness promoting gene, ID2, and diminished self-renewal ability of DCIS cells. Importantly, we screened a library containing 390 natural compounds and identified toyocamycin as a compound that selectively inhibited the growth of DCIS with low expression of IPW, while it did not affect DCIS with high IPW expression. Toyocamycin also suppressed genes associated with self-renewal ability and inhibited DCIS growth in vivo. CONCLUSION: Our findings revealed a critical role of the IPW-miR-29c-ID2 axis in DCIS formation and suggested potential clinical use of toyocamycin for the treatment of DCIS.

Exosomal miR-19a and IBSP cooperate to induce osteolytic bone metastasis of estrogen receptor-positive breast cancer.

Bone metastasis is an incurable complication of breast cancer. In advanced stages, patients with estrogen-positive tumors experience a significantly higher incidence of bone metastasis (>87%) compared to estrogen-negative patients (<56%). To understand the mechanism of this bone-tropism of ER+ tumor, and to identify liquid biopsy biomarkers for patients with high risk of bone metastasis, the secreted extracellular vesicles and cytokines from bone-tropic breast cancer cells are examined in this study. Both exosomal miR-19a and Integrin-Binding Sialoprotein (IBSP) are found to be significantly upregulated and secreted from bone-tropic ER+ breast cancer cells, increasing their levels in the circulation of patients. IBSP is found to attract osteoclast cells and create an osteoclast-enriched environment in the bone, assisting the delivery of exosomal miR-19a to osteoclast to induce osteoclastogenesis. Our findings reveal a mechanism by which ER+ breast cancer cells create a microenvironment favorable for colonization in the bone. These two secreted factors can also serve as effective biomarkers for ER+ breast cancer to predict their risks of bone metastasis. Furthermore, our screening of a natural compound library identifies chlorogenic acid as a potent inhibitor for IBSP-receptor binding to suppress bone metastasis of ER+ tumor, suggesting its preventive use for bone recurrence in ER+ patients.

Evaluation of the association between olecranon fracture and radial head subluxation or annular ligament displacement in children.

Olecranon fractures are seen substantially more often in children than in adult and are potentially occult in nature. We noticed this fracture pattern in two cases of delayed Monteggia fracture. Our study purpose was to confirm whether olecranon fracture is associated with radial head subluxation or annular ligamentous displacement in children. In addition, we have developed an effective and simple approach to avoid serious treatment-related complications as much as possible. Forty-eight pediatric patients with olecranon fracture and normal radiocapitellar alignment on radiography were enrolled. All patients' fingers, forearms and elbows were examined carefully, and treated with a modified radial head reduction approach and then cast immobilization. MRI of the affected elbow was performed in 16 symptomatic patients. Overall, 70.83% of patients had a positive clinical finding of radial head subluxation. These symptomatic patients presented with similar clinical findings that typically included painful finger movement actively or passively and movement limitation of forearm and elbow. MRI showed that annular ligaments were interposed and trapped in the radiohumeral joint. In 34 symptomatic patients, 91.18% of them achieved fair radial head reduction during the first reduction attempt. Herein, 95.85 and 100% of patients reported excellent and satisfactory outcomes, respectively. Radial head subluxation occurred in most children with an olecranon fracture. We highly suggest performing a careful physical examination to identify this fracture pattern. Early reduction of the radial head with the modified approach may be a simple and primary option for emergency room doctors.

Regucalcin promotes dormancy of prostate cancer.

Prostate cancer is one of the leading causes of mortality in men. The major cause of death in prostate cancer patients can be attributed to metastatic spread of disease or tumor recurrence after initial treatment. Prostate tumors are known to remain undetected or dormant for a long period of time before they progress locoregionally or at distant sites as overt tumors. However, the molecular mechanism of dormancy is yet poorly understood. In this study, we performed a differential gene expression analysis and identified a gene, Regucalcin (RGN), which promotes dormancy of prostate cancer. We found that cancer patients expressing higher level of RGN showed significantly longer recurrence-free and overall- survival. Using a doxycycline-inducible RGN expression system, we showed that ectopic expression of RGN in prostate tumor cells induced dormancy in vivo, while following suppression of RGN triggered recurrence of tumor growth. On the other hand, silencing RGN in LNCap cells promoted its outgrowth in the tibia of mice. Importantly, RGN promoted multiple known hallmarks of tumor dormancy including activation of p38 MAPK, decrease in Erk signaling and inhibition of FOXM1 expression. Furthermore, we found that RGN significantly suppressed angiogenesis by increasing secretory miR-23c level in the exosomes. Intriguingly, FOXM1 was found to negatively regulate miR-23c expression in prostate cancer. In addition, we identified 11 RGN downstream target genes that independently predicted longer recurrence-free survival in patients. We found that expression of these genes was regulated by FOXM1 and/or p38 MAPK. These findings suggest a critical role of RGN in prostate cancer dormancy, and the utility of RGN signaling and exosomal miR-23c as biomarkers for predicting recurrence.

TRIM3 inhibits P53 signaling in breast cancer cells.

BACKGROUND: Beast cancer is the most common women cancer worldwide, while two third of them are ER alpha positive breast cancer. Among the ER alpha positive breast cancer, about 80% are P53 wild type, indicating the potential tumor suppression role in ER alpha positive breast cancer. Since P53 is an important safeguard to inhibit cell malignant transformation, reactivating P53 signaling could a plausible approach to treat breast cancer. METHODS: TRIM3 protein levels were measured by western blot, while the P53 classical target genes were measured by real-time PCR. WST1 assay were used to measure cell proliferation, while cleaved caspase-3 was used to detect cell apoptosis. Protein stability and ubiquitin assay were used to detect the P53 protein ubiquitin and stability. The immuno-precipitation assays were used to detect the protein interactions. Immuno-staining was used to detect the protein localization of P53 and TRIM3, while the ubiquitin-based immuno-precipitation assays were used to detect the specific ubiquitination manner of P53. RESULTS: In our study, we identified TRIM3 as an endogenous inhibitor for P53 signaling. TRIM3 depletion inhibited breast cancer cell proliferation and promoted apoptosis. In addition, TRIM3 depletion increased P53 protein level in breast cancer cell. Further investigation showed that TRIM3 could associate with P53 and promote P53 K48-linked ubiquitination and degradation. CONCLUSION: Our study identified a novel post-translational modification mechanism between TRIM3 and P53. TRIM3 depletion or blockage could be a promising strategy to rescue P53 signaling and inhibit breast cancer progression.

Circular RNA circ-ZEB1 acts as an oncogene in triple negative breast cancer via sponging miR-448.

BACKGROUND: Circular RNAs (circRNAs) play an important role in tumor development. The miRNA sponge is a common role played by circRNAs in various tumors, including breast cancer. OBJECTIVE: This study aimed to explore the role of circ-ZEB1 in the proliferation and apoptosis of triple negative breast cancer (TNBC) cells. METHODS: The expressions of several circRNAs which were predicted to be bound with miR-448 were detected in 30 clinical TNBC tumor tissues and paired paracancer tissues. The cell counting kit-8 assay was performed to detect the TNBC cell proliferation. The TNBC cell apoptosis was detected using the TUNEL assay. The binding between circ-ZEB1 and miR-448, as well as between miR-448 and eukaryotic elongation factor 2 kinase (eEF2 K), was detected using the RNA pull-down assay and/or the luciferase reporter assay. The effect of circ-ZEB1 knockdown on TNBC tumor growth was detected using the mouse xenograft model. RESULTS: Compared with normal tissues and breast epithelial cells, the expression of circ-ZEB1 was markedly higher in TNBC tumor tissues and tumor cell lines. The small hairpin RNA-mediated circ-ZEB1 knockdown inhibited TNBC cell proliferation and induced cell apoptosis. The RNA pull-down assay and the luciferase reporter assay confirmed the binding between circ-ZEB1 and miR-448, as well as between miR-448 and eEF2 K. The knockdown of circ-ZEB1 was proven to inhibit TNBC cell proliferation and tumor growth via releasing miR-448, and subsequently reducing the expression of the miR-448 target, eEF2 K. CONCLUSION: In conclusion, our findings identified a new functional circ-ZEB1 in TNBC tumorigenesis, and revealed the important regulatory role of circ-ZEB1 via sponging miR-448, providing a novel insight for TNBC pathogenesis.

Exosome-mediated transfer of long noncoding RNA H19 induces doxorubicin resistance in breast cancer.

Development of the acquired resistance is one major obstacle during chemotherapy for cancer patients. Exosomes mediate intercellular communication and cause environmental changes in tumor progression by transmitting active molecules. In this study, the role of long noncoding RNA H19 within exosomes is elucidated in terms of regulating doxorubicin (DOX) resistance of breast cancer. As a result, increased H19 expression was observed in DOX-resistant breast cancer cells in comparison with the corresponding parental cells. Suppression of H19 significantly lowered DOX resistance by decreasing cell viability, lowering colony-forming ability, and inducing apoptosis. Moreover, extracellular H19 could be moved to sensitive cells via being incorporated into exosomes. Treating sensitive cells with exosomes from resistant cells increased the chemoresistance of DOX, while downregulation of H19 in sensitive cells abated this effect. Taken together, H19 could be delivered by exosomes to sensitive cells, leading to the dissemination of DOX resistance. Our finding highlights the potential of exosomal H19 as a molecular target to reduce DOX resistance.

Recommendations for control and prevention of infections for pediatric orthopedics during the epidemic period of COVID-19.

The outbreak of Coronavirus Disease 2019 (COVID-19) caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) emerged and spread rapidly throughout the world. As of February 29, 2020, 79 389 cases of COVID-19 have been reported, and the outbreak is linked to 2838 deaths. The population is generally susceptible to the disease, and differences in incubation periods after infection exist among individuals. These two aspects of COVID-19 pose significant challenges to pediatric orthopedic diagnosis and treatment. As a dedicated center for managing pediatric cases of SARS-CoV-2 in Shanghai, our hospital has mobilized all branches and departments to undertake joint actions for scientific prevention and control, precise countermeasure and comprehensive anti-epidemic efforts. Combined with our experience, we have consulted the relevant national regulations and the latest research advances and have formulated the prevention and control measures of SARS-CoV-2 infection, including outpatient, emergency, inpatient and surgical cares, for clinical practices of pediatric orthopedics according to the physicochemical properties of SARS-CoV-2. It may serve as practical references and recommendations for managing SARS-CoV-2 infection in other pediatric specialties and in other hospitals.

Baicalin Inhibits Cell Viability, Migration and Invasion in Breast Cancer by Regulating miR-338-3p and MORC4.

BACKGROUND: Baicalin is a natural compound from the roots of Scutellaria lateriflora Georgi, which plays anti-cancer role in multiple cancers. However, the exact role and potential underlying mechanism of baicalin in breast cancer (BC) remain poorly understood. METHODS: Thirty BC patients were recruited in this study. MCF-10A, MCF-7 and MDA-MB-231 cells were used to investigate the anti-cancer role of baicalin in vitro. Cell viability, migration, invasion and apoptosis were measured by MTT, trans-well and flow cytometry, respectively. The expression levels of microRNA-338-3p (miR-338-3p) and microrchidia family CW-type zinc-finger 4 (MORC4) were measured by quantitative real-time polymerase chain reaction or Western blot. The interaction between miR-338-3p and MORC4 was explored by luciferase reporter assay and RNA immunoprecipitation. RESULTS: We found that Baicalin treatment inhibited cell viability, migration and invasion but promoted apoptosis of BC cells. The expression of miR-338-3p was decreased in BC tissues and cells and miR-338-3p overexpression suppressed cell viability, migration and invasion but induced apoptosis. MiR-338-3p expression was reversed by baicalin exposure and inhibition of miR-338-3p attenuated the role of baicalin in viability, apoptosis, migration and invasion. MORC4 mRNA level was increased in BC tissues and cells, which was decreased by baicalin exposure. MORC4 was a target of miR-338-3p and its overexpression alleviated the effect of miR-338-3p on cell viability, apoptosis, migration and invasion. CONCLUSION: In conclusion, baicalin suppressed cell viability, migration and invasion but promoted apoptosis in BC cells by regulating miR-338-3p and MORC4, indicating the promising pharmacological value of baicalin in BC treatment.

miR-506 attenuates methylation of lncRNA MEG3 to inhibit migration and invasion of breast cancer cell lines via targeting SP1 and SP3.

BACKGROUND: Breast cancer has been the first death cause of cancer in women all over the world. Metastasis is believed to be the most important process for treating breast cancer. There is evidence that lncRNA MEG3 functions as a tumor suppressor in breast cancer metastasis. However, upstream regulation of MEG3 in breast cancer remain elusive. Therefore, it is critical to elucidate the underlying mechanism upstream MEG3 to regulate breast cancer metastasis. METHODS: We employed RT-qPCR and Western blot to examine expression level of miR-506, DNMT1, SP1, SP3 and MEG3. Besides, methylation-specific PCR was used to determine the methylation level of MEG3 promoter. Wound healing assay and transwell invasion assay were utilized to measure migration and invasion ability of breast cancer cells, respectively. RESULTS: SP was upregulated while miR-506 and MEG3 were downregulated in breast tumor tissue compared to adjacent normal breast tissues. In addition, we found that miR-506 regulated DNMT1 expression in an SP1/SP3-dependent manner, which reduced methylation level of MEG3 promoter and upregulated MEG3 expression. SP3 knockdown or miR-506 mimic suppressed migration and invasion of MCF-7 and MDA-MB-231 cells whereas overexpression of SP3 compromised miR-506-inhibited migration and invasion. CONCLUSIONS: Our data reveal a novel axis of miR-506/SP3/SP1/DNMT1/MEG3 in regulating migration and invasion of breast cancer cell lines, which provide rationales for developing effective therapies to treating metastatic breast cancers.

LncRNA SNHG1 regulates the differentiation of Treg cells and affects the immune escape of breast cancer via regulating miR-448/IDO.

OBJECTIVE: To investigate the mechanism of lncRNA SNHG1 in the immune escape of breast cancer (BC). METHODS: SNHG1, miR-448 and IL-10 levels were evaluated by qRT-PCR. The protein levels of IDO and Foxp3 were measured by Western blot. SNHG1 and miR-448 interaction was tested by RIP assay and RNA pull-down assay. MiR-448 and IDO interaction was observed by luciferase reporter assay. RESULTS: Compared with CD4+T cells, miR-448 expression in CD4+ TIL cells was decreased, while the expression of SNHG1, IDO, IL-10 and Foxp3 were increased. Moreover, SNHG1 directly contacted with miR-448, which could negatively regulate IDO. In cells treated with siRNA-SNHG and miR-448 inhibitor, interference SNHG1 up-regulated miR-448 expression and down-regulated IDO expression, while miR-448 inhibitor reversed this effect. In addition, miR-448 inhibitor reversed the inhibitory effect of siRNA-SNHG1 on Treg cell differentiation, and siRNA-SNHG1 could reduce tumor volume and down-regulated the expressions of SNHG1, IL-10, IDO and Foxp3. CONCLUSION: Interference SNHG1 could inhibit the differentiation of Treg cells by promoting miR-448 expression and reducing IDO level, thereby impeding the immune escape of BC.

TOX high mobility group box family member 3 rs3803662 and breast cancer risk: A meta-analysis.

AIMS: Some studies suggested that TOX high mobility group box family member 3 (TOX3) rs3803662 polymorphism was associated with the risk of breast cancer. However, the results were controversy. Therefore, in order to derive a more comprehensive estimation of the association between TOX3 rs3803662 polymorphism and breast cancer risk, we conducted a meta-analysis to investigate this relationship. MATERIALS AND METHODS: An electronic literature search was conducted using the following database: PubMed, EMBASE, and China National Knowledge Infrastructure till to March 31, 2015. The strength of the associations between the TOX3 rs3803662 polymorphism and breast cancer risk in per alle model was measured by odds ratios (ORs) and 95% confidence intervals (CIs). RESULTS: A statistically significant association between TOX3 rs3803662 polymorphism and breast cancer risk was fond. The data showed that TOX3 rs3803662 polymorphism could increase the risk of breast cancer (OR = 1.20; 95% CI: 1.16-1.25; P < 0.00001). In the subgroup analysis of race, Caucasians, Asians, and Hispanics also showed increased breast cancer risk (OR = 1.21; 95% CI: 1.17-1.25; P < 0.00001; OR = 1.20; 95% CI: 1.08-1.33; P = 0.0004; OR = 1.32; 95% CI: 1.12-1.57; P = 0.001). However, African-Americans with TOX3 rs3803662 polymorphism showed decreased breast cancer risk (OR = 0.95; 95% CI: 0.86-1.04; P = 0.28), although the result was not significant. When considered estrogen receptor (ER) status, we found that ER + subjects and ER - subjects all had increased breast cancer risk, if they carried this polymorphism (OR = 1.27; 95% CI: 1.19-1.35; P < 0.00001; OR = 1.12; 95%CI: 1.08-1.17; P < 0.00001). Similarly, both progesterone receptor-positive (PR +) subjects and PR - subjects all showed increased breast cancer risk, if they carried this polymorphism (OR = 1.32; 95% CI: 1.17-1.49; P < 0.00001; OR = 1.15; 95% CI: 1.09-1.23; P < 0.00001). CONCLUSIONS: This meta-analysis suggested that TOX3 rs3803662 polymorphism was associated with increased breast cancer risk.

Leverage application on Gartland type IV supracondylar humeral fracture in children.

PURPOSE: Although the most complex management of Gartland type IV supracondylar humeral fracture (SCHF) due to instability, the gold standard of initial treatment remains closed reduction and percutaneous pinning. However, open reduction was inevitable in most published studies. This study reports the outcome of treatment by leverage-assisted closed reduction. METHOD: Twenty-seven patients were diagnosed as Gartland type IV SCHF during surgery in 214 preoperative Gartland type III fractures. Leverage-assisted reduction with percutaneous lateral pinning was done in these patients after failure of close reduction. Evaluations were performed with radiographic examination, clinical assessment and Flynn's criteria by interview and physical examination. RESULT: All 27 patients obtained acceptable reduction by leverage-assisted close reduction and percutaneous pinning. The average follow-up was 23.6 (18-30 months). There was no neurovascular complication, infection, nonunion, myositis ossificans or Volkmann's contracture. Evaluation of Baumann's angle was towards varus (74-74.2°). There was no significant difference (p = 0.1876). Flynn's criteria were excellent in 22 (81.5 %) patients, good in four (14.8 %) and fair in one (3.7 %). The rate of excellent and good outcome was 96.3 % and of satisfactory 100 %. CONCLUSION: We recommend leverage-assisted closed reduction as an option before open reduction in type IV SCHF, not only for gold standard management but also because of satisfactory outcomes and the low incidence of major complications.

MicroR-760 suppresses cancer stem cell subpopulation and breast cancer cell proliferation and metastasis: By down-regulating NANOG.

BACKGROUND AND OBJECTIVE: Emerging evidences suggest that cancer stem cells are responsible for tumor aggressive, metastasis and therapeutic resistance. To data, the mechanism underlying breast cancer stem cell (BCSC) population within tumor metastasis remains to be fully elucidated. The current study was to investigate the potential role of microRNA-760 (miR-760) and its associated target gene in population and metastasis of BCSC. METHODS: Characteristic BCSCs surface markers (CD44(+)/CD24(-/low)) were determined by flow cytometry in breast cancer MCF-7 and BT-549 cells. Quantitative RT-PCR was used to evaluate miR-760 and NANOG mRNA expression. Expression of NANOG protein was determined using western blot. Cell proliferation was determined by MTT assay. The model of breast cancer cell xenograft was used to evaluate the effect of miR-760 on tumor growth. RESULTS: BT-549 cell has substantially more CD44(+)/CD24(-/low) subpopulation than MCF-7 cell. Moreover, BT-549 cell expressed lower level of miR-760 and higher level of NANOG than MCF-7cell. By result from cellular miR-760 modulation, we found that miR-760 overexpression suppressed CD44(+)/CD24(-/low) population as well as inhibited cell proliferation and migration of BT-549. On the contrary, knockdown of miR-760 promoted CD44(+)/CD24(-/low) population and migration of MCF-7 cells. By luciferase reporter assay, miR-760 was proved to be functional associated with NANOG via regulating its expression. This functional interaction was showed to be involved in controlling proliferation and migration of MCF-7 and BT-549 cell. CONCLUSION: These data suggest that the target of miR-760/NANOG axis may represent a new therapeutic approach to suppress breast cancer stem cell subpopulation thereby prevent cancer metastasis.