Staged Immediate Nipple Reconstruction With Tube Flap in Immediate Deep Inferior Epigastric Artery Perforator Flap Breast Reconstruction.

BACKGROUND: In the setting of immediate breast reconstruction by deep inferior epigastric artery perforator (DIEP) flap, the excessive DIEP flap skin is de-epithelialized and then buried under the mastectomy skin. In this study, by virtue of tube flap technique, we hypothesize that the skin supposed to be abandoned could be transferred to the apex of reconstructed breast mound for nipple reconstruction. METHODS: A total of 60 female patients were recruited between January 2019 and December 2020. All these patients underwent mastectomy including nipple-areola complex and immediate DIEP flap breast reconstruction. A ladder-shaped pedicled flap was raised from the DIEP flap and rolled into a tube. The free end of tube flap was inset into the future nipple position of the reconstructed breast mound 1 week later. After revascularization for 1 month, we divided the previous pedicle and used the tube on the apex of the breast mound to recreate a new nipple. RESULTS: All reconstructed breasts and nipples survived well postoperatively. The average nipple projection was 12.5 ± 2.0 mm immediately after the surgery, which gradually decreased to 9.4 ± 1.5 mm at 1-year follow-up, with the projection loss from the initial measurement as 24.9% ± 1.8%. In total, 51 patients considered the overall impression of breast and nipple reconstruction to be very good or good. CONCLUSIONS: We provided an ideal technique that could improve the maintenance of reconstructed nipple projection and have aesthetically acceptable outcomes, without DIEP flap tissue loss, breast mound distortion, or additional scars.

KRT15 in early breast cancer screening and correlation with HER2 positivity, pathological grade and N stage.

Objective: This study was designed to explore KRT15 dysregulation and its correlation with clinical characteristics among ductal carcinoma in situ (DCIS), DCIS with microinvasion (DCIS-MI) and invasive breast cancer (IBC) patients. Methods: KRT15 from lesion samples of 50 DCIS patients, 48 DCIS-MI patients and 50 IBC patients was detected by immunohistochemistry. Results: KRT15 discriminated IBC patients from DCIS patients (area under the curve [AUC] = 0.895; 95% CI = 0.836-0.954) and DCIS-MI patients (AUC = 0.707; 95% CI = 0.606-0.808). In DCIS patients, KRT15 was negatively correlated with pathological grade (p = 0.015). In DCIS-MI patients, KRT15 was positively related to estrogen receptor positivity but negatively associated with Ki-67 (both p < 0.05). In IBC patients, KRT15 was negatively linked to HER2 positivity, histological grade, N stage and tumor node metastasis stage (all p < 0.05). Conclusion: KRT15 assessment may help with early breast cancer screening.

Stereochemical insights into structurally diverse lignanamides from the herbs of Solanum lyratum Thunb.

A chemical investigation of Solanum lyratum Thunb. (Solanaceae) afforded six pairs of enantiomeric lignanamides consisting of twelve undescribed compounds, along with two undescribed racemic mixtures, and the separations of the enantiomers were accomplished by chiral-phase HPLC. The structures of these undescribed compounds were elucidated by the analysis of spectroscopic data, NMR and electronic circular dichroism calculations. All isolated compounds were assessed for neuroprotective activities in H2O2-induced human neuroblastoma SH-SY5Y cells, and acetylcholinesterase (AChE) inhibitory activities. Among tested isolates, some enantiomeric lignanamides exhibited conspicuous neuroprotective effects and AChE inhibitory effect.

In-situ-reduced synthesis of cyano group modified g-C3N4/CaCO3 composite with highly enhanced photocatalytic activity for nicotine elimination.

Graphite carbon nitride has many excellent properties as a two-dimensional semiconductor material so that it has a wide application prospect in the field of photocatalysis. However, the traditional problems such as high recombination rate of photogenerated carriers limit its application. In this work, we introduce nitrogen deficiency into g-C3N4 to solve this problem a simple and safe in-situ reduction method. g-C3N4/CaCO3 was obtained by a simple and safe one-step calcination method with industrial-grade micron particles CaCO3. Cyano group modification was in-situ reduced during the thermal polymerization process, which would change the internal electronic structure of g-C3N4. The successful combination of g-C3N4 and CaCO3 and the introduction of cyanide have been proved by Fourier transform infrared spectroscopy and X-ray photoelectron spectrometer. The formation of the cyano group, an electron-absorbing group, promotes the effective separation of photogenic electron hole pairs and inhibits the recombination of photogenic carriers. These advantages result in the generation of more •O2- and 1O2 in the catalytic system, which increases the photocatalytic efficiency of nicotine degradation by ten times. Furthermore, the degradation process of nicotine has been studied in this work to provide a basis for the degradation of nicotine organic pollutants in the air.

Potential of blood exosomal ENAH, SEPT9, EGF, MMP-9 and CXCL8 for the early screening of breast cancer.

Exosomal contents have been recognized as candidate biomarkers for cancer screening and prognosis. The current study aimed to evaluate the potential of the expression levels of exosomal enabled homolog (ENAH), septin 9 (SEPT9), epidermal growth factor (EGF), matrix metalloproteinase-9 (MMP-9) and C-X-C motif chemokine ligand 8 (CXCL8) in the blood for the early screening of breast cancer. Therefore, exosomes were extracted and purified from the peripheral blood of 47 patients with breast cancer, 63 disease controls (DCs) and 33 healthy controls (HCs). Subsequently, the exosomal mRNA expression levels of ENAH, SEPT9, EGF, MMP-9 and CXCL8 were detected by reverse transcription-quantitative polymerase chain reaction. The results showed that the exosomal levels of ENAH and EGF were significantly higher in patients with breast cancer compared with DCs and HCs (both P<0.001). In addition, receiver operating characteristic curves revealed that exosomal ENAH was able to discriminate patients with breast cancer from DCs [area under the curve (AUC), 0.841] and HCs (AUC, 0.859). However, exosomal EGF was only able to discriminate patients with breast cancer from HCs (AUC, 0.776). Furthermore, the levels of exosomal SEPT9 were lower in patients with breast cancer compared with DCs and HCs (P=0.021), and exosomal SEPT9 expression levels exhibited good potential in the discrimination of patients with breast cancer from DCs (AUC, 0.717) and HCs (AUC, 0.830). However, no significant difference was detected in exosomal levels of MMP-9 and CXCL8 among the three groups, and these RNAs showed no discriminative ability. In addition, in patients with breast cancer, the exosomal levels of ENAH were associated with molecular subtypes (P=0.010), while those of MMP-9 were associated with a Ki-67 index of ≥30% (P=0.011). In conclusion, the exosomal levels of ENAH, SEPT9 and EGF in blood samples were able to identify patients with breast cancer, thus providing a novel approach for the early screening of breast cancer.

Standardized Skin Flap Warming Effectively Improves Flap Survival without Obstructing Temperature Monitoring after DIEP.

OBJECTIVE: This study aimed to determine whether skin flap warming after an operation interferes with temperature monitoring. The postoperative nursing workflow of subabdominal deep inferior epigastric artery perforator (DIEP) flap breast reconstruction was optimized. METHODS: A retrospective analysis involving 69 patients who received one-stage breast reconstruction at the Huashan Hospital from July 2017 to December 2019 was performed. The postoperative physical care of patients, including flap temperature monitoring and flap warming, was reviewed. RESULTS: All patients had successful operations. After surgery, all flaps were warmed following the standard protocol. Abnormal temperature and compromised circulation of flaps were observed in three of the patients. These patients received re-exploration surgery and all three flaps survived. A postoperative follow-up shows a high level of patient satisfaction in most cases. CONCLUSIONS: The appropriate warming of transplanted flaps did not interfere with temperature monitoring. This helped determine whether there was compromised circulation, leading to increased skin flap survival and improved patient satisfaction.

Boronic derivatization-based strategy for monoacylglycerol identification, isomer annotation and quantification.

Monoacylglycerols (MAGs) are important signaling molecules involved in various diseases. However, it is challenge for direct detection of MAGs and isomers. Additionally, difficulties in isomer annotation hinders the comprehensive profiling of MAGs and hampers revealing isomers' contributions to diseases. Herein, a boronic derivatization-based strategy was developed for unambiguous identification, isomer annotation and quantification of MAGs in biological samples. 3-Nitrophenylboronic acid was selected as the derivatization reagent owing to its rapid and selective reactivity toward cis-diol moiety. First, a prediction model was established for MAG identification by the integration of m/z, isotopic distribution of boron, and retention time attributed by the carbon chain length and number of double bonds, which solved the difficulty of obtaining MAG standards. In addition, the designed derivatization reaction enabled the capture of thermally unstable sn-2 MAG isomers to ensure the chromatographic separation and direct MS detection. What's more, distinguished fragmentation patterns were discovered for derivatized MAG isomers, which allowed a novel and unambiguous isomer annotation. Furthermore, by considering the availability of standards, the quantification of MAGs was based on the development of calibration curves or relative quantification by internal standard. On this basis, the developed strategy was utilized for MAG identification and quantification in breast cancer samples, which suggested that MAGs could be regarded as potential biomarkers in breast cancer diagnosis or as indicators to trace the process of chemotherapy. It also helped make the puzzle complete by revealing that only one single isomer associated with the onset of disease was possible, instead of regarding them as a whole. Therefore, the boronic derivatization-based strategy facilitated the unambiguous identification, annotation and quantification of MAGs and isomers in biofluids, and would be beneficial for the mechanism studies of related diseases.

OGT regulated O-GlcNAcylation promotes papillary thyroid cancer malignancy via activating YAP.

The incidence of thyroid cancer is growing rapidly during the past decades worldwide. Although most thyroid tumors are curable, some patients diagnosed with distant metastases are associated with poor prognosis. The molecular mechanisms underlying these cases are still largely unknown. Here we found that the upregulated O-Linked N-Acetylglucosamine Transferase (OGT) expression and O-GlcNAcylation (O-GlcNAc) modification in papillary thyroid cancer (PTC) were essential in tumor growth and metastasis. Mass spectrometry analysis showed that YAP was the effector protein modified by OGT. In details, YAP Ser109 O-GlcNAcylation promoted the malignant phenotypes in PTC cells by inducing YAP Ser127 dephosphorylation and activation. Our work clearly showed the critical role of OGT and YAP played in PTC tumors and made it possible for us to seek the clinical potential of manipulating OGT/YAP activity in PTC targeted therapies. These findings also confirmed OGT worked in collaboration with classical Hippo pathway kinases as an upstream regulator of YAP in PTC tumors.

RNA-binding protein QKI suppresses breast cancer via RASA1/MAPK signaling pathway.

BACKGROUND: RNA-binding protein Quaking (QKI) has been linked with the pathogenesis and development of various human malignancies. Herein, we explored the particular role of QKI in breast cancer (BC) progression. METHODS: The methods employed in the study included public dataset analysis, western blot, quantitative real-time PCR (qRT-PCR), cell count kit-8 (CCK8) assay, colony formation assay, flow cytometric analysis, RNA immunoprecipitation (RIP), messenger RNA (mRNA) stability assay, QKI overexpression and knockdown, and Ras p21 protein activator 1 (RASA1) knockdown. RESULTS: Aberrant expression levels of QKI and RASA1 were detected in BC and compared with those in noncancerous tissues. A moderately positive correlation between QKI and RASA1 was verified within BC tissues. Low expression of QKI was associated with positive estrogen receptor (ER), progesterone receptor (PR) and human epidermal growth factor receptor 2 (HER2) status, non-triple-negative breast cancer (TNBC), non-basal-like BC, and poor clinical outcomes in BC patients. QKI overexpression suppressed BC cell proliferation and colony formation, and arrested cell cycle at G1 phase. RIP assay and mRNA stability assay confirmed that QKI directly bound to RASA1 transcript and increased its stability, thus inactivating the MAPK pathway and inhibiting BC progression. RASA1 knockdown could partly attenuate the inhibitory effect of QKI on BC cell proliferation via activating the mitogen-activated protein kinase (MAPK) pathway. CONCLUSIONS: QKI, which was frequently downregulated in BC, could significantly inhibit cell proliferation and arrest cell cycle at G1 phase by binding and enhancing RASA1 mRNA expression. Low expression of QKI was prominently associated with unfavorable clinical outcomes in BC patients, indicating the prognostic value of QKI in BC.

SLC34A2 simultaneously promotes papillary thyroid carcinoma growth and invasion through distinct mechanisms.

Thyroid cancer is the fastest growing cancer among all solid tumors in recent decades. Papillary thyroid carcinoma (PTC) is the most predominant type of thyroid cancer. Around 30% of PTC patients with distant metastases and local invasion receive poor prognosis. Thus, the identification of new druggable biological targets is of great importance. Accumulating evidence indicates that solute carrier family numbers have emerged as obligate effectors during the progression of multiple malignancies. Here, we uncovered the functional significance, molecular mechanisms, and clinical impact of solute carrier family 34 member A2 (SLC34A2) in PTC. SLC34A2 was markedly overexpressed in PTC tissues at both mRNA and protein levels compared with matched adjacent normal tissues due to promoter hypomethylation mediated by the DNA methyltransferase 3 beta (DNMT3B). Furthermore, a series of in vivo and in vitro gain- or loss-of-functional assays elucidated the role of SLC34A2 in boosting cell proliferation, cell cycle progression, migration, invasion, and adhesion of PTC cells. Using immunoprecipitation and mass spectrometry, we discovered that SLC34A2 bound to the actin-binding repeats domain of Cortactin (CTTN), thereby inducing the invadopodia formation of PTC cells to promote the metastasis potential of PTC cells. Besides, our mechanistic studies, as well as gene set enrichment analysis (GSEA), have pinpointed the PTEN/AKT/FOXO3a pathway as a major signaling functioning downstream of SLC34A2 regulated cell growth. Taken together, our results highlighted that SLC34A2 plays a pivotal oncogenic role during carcinogenesis and metastasis through distinct mechanisms in PTC.

Values of 5mC, 5hmC, and TET2 for identifying the presence and progression of breast precancerous lesion.

BACKGROUND: This study aimed to evaluate the correlations of 5-methylcytosine (5mC), 5-hydroxymethylcytosine (5hmC), and ten-eleven translocation enzyme 2 (TET2) expressions in lesion tissue with histological classification of breast precancerous lesion. METHODS: Eighty-three patients with breast ductal intraepithelial neoplasia (DIN), 20 patients with breast ductal carcinoma in situ with microinvasion (DCIS-MI), and 10 patients with invasive breast cancer were included. Histological classification of the DIN patients was classified as DIN1A, DIN1B, DIN1C, DIN2, and DIN3. 5mC, 5hmC, and TET2 expressions in lesion tissues from biopsy were assessed by immunohistochemistry (IHC) assay. RESULTS: 5hmC and TET2 were negatively associated with histological classification as validated by both IHC score and IHC semi-quantification expression grades in total patients (all P < .05); however, no correlation of 5mC with histological classification was found (all P > .05). 5mC (P = .004) was negatively but 5hmC (P < .001) was positively correlated with TET2, while no association of 5mC with 5hmC was discovered in total patients (P = .078). In addition, 5mC was positively associated with ER expression in total patients (P = .040). In subgroups, 5mC was negatively correlated with 5hmC in DIN1C patients (P = .023) and invasive cancer patients (P = .044), and 5mC was negatively associated with TET2 in DIN1B patients (P = .004) as well as DCIS-MI patients (P = .003). CONCLUSION: 5hmC and TET2 have the potentials to serve as biomarkers that could assist in the identification of presence and progression of breast precancerous lesion.

Prognostic value of epithelial-mesenchymal transition related genes: SLUG and QKI in breast cancer patients.

Snail family zinc finger 2 (SLUG) is related to epithelial-mesenchymal transition (EMT). Quaking (QKI) is an RNA binding protein and has been indicated to have a relationship with EMT by recent studies. The prognostic value of SLUG and QKI in breast cancer patients still needs exploration. We conducted Immunohistochemistry (IHC) to evaluate the protein expression of SLUG and QKI and the prognostic value in 108 breast cancer (BC) patients. The Bc-GenExMiner database was used to compare the mRNA levels of two genes in different subgroups of BC patients. Kaplan-Meier plotter were used for survival data of SLUG and QKI gene. We also mined the cBioPortal database for co-expression analysis of QKI and EMT markers. Our results suggested that patients with higher expression of SLUG and QKI showed shorter overall survival time. The mRNA level of SLUG and QKI were higher in ER negative, PR negative, ≤ 51 y, and TNBC patients. SLUG mRNA showed no survival significance, while higher QKI mRNA expression level was correlated with worse clinical outcome in Kaplan-Meier Plotter database. The cBioPortal database showed that QKI was correlated to SLUG as well as other EMT markers like TWIST2, VIM, and ZEB2. QKI was indicated to be a potential prognostic marker for BC patients, and combined expression of SLUG and QKI showed the best prognostic value. Co-expression analysis indicated that QKI was likely to have a correlation with SLUG and EMT.

A simple boronic acid-based fluorescent probe for selective detection of hydrogen peroxide in solutions and living cells.

An approach of high sensitivity and selectivity for hydrogen peroxide (H2O2) detection is highly demanded due to its important roles in regulating diverse biological process. In this work, we introduced an easily synthesized fluorescent "turn off" probe, BNBD. It is designed based on the core structure of 4-chloro-7-nitrobenzofurazan as a fluorophore and incorporated with a specific H2O2-reactive group, aryl boronate, for sensitive and selective detection of H2O2. We demonstrated its selectivity by incubating the probe with other types of ROS, and measured the limit of detection of BNBD as 1.8 nM. BNBD is also conducive to H2O2 detection at physiological conditions. We thus applied it to detect both exogenous and endogenous changes of H2O2 in living cells by confocal microscopy, supporting its future applications to selectively monitor H2O2 levels and identify H2O2-related physiological or pathological responses from live cells or tissues in the near future.

Solute carrier family 35 member F2 is indispensable for papillary thyroid carcinoma progression through activation of transforming growth factor-ß type I receptor/apoptosis signal-regulating kinase 1/mitogen-activated protein kinase signaling axis.

Solute carrier family members control essential physiological functions and are tightly linked to human diseases. Solute carrier family 35 member F2 (SLC35F2) is aberrantly activated in several malignancies. However, the biological function and molecular mechanism of SLC35F2 in papillary thyroid carcinoma (PTC) are yet to be fully explored. Here, we showed that SLC35F2 was prominently upregulated in PTC tissues at both protein and mRNA expression level compared with matched adjacent normal tissues. Besides, the high expression of SLC35F2 was significantly associated with lymph node metastasis in patients with PTC. CRISPR/Cas9-mediated knockout of SLC35F2 attenuated the tumorigenic properties of PTC, including cell proliferation, migration and invasion and induced G1 phase arrest. In contrast, ectopic expression of SLC35F2 brought about aggressive malignant phenotypes of PTC cells. Moreover, SLC35F2 expedited the proliferation and migration of PTC cells by targeting transforming growth factor-ß type I receptor (TGFBR1) and phosphorylation of apoptosis signal-regulating kinase 1 (p-ASK-1), thereby activating the mitogen-activated protein kinase signaling pathway. The malignant behaviors induced by overexpression of SLC35F2 could be abrogated by silencing of TGFBR1 using a specific inhibitor. We conducted the first study on SLC35F2 in thyroid cancer with the aim of elucidating the functional significance and molecular mechanism of SLC35F2. Our findings suggest that SLC35F2 exerts its oncogenic effect on PTC progression through the mitogen-activated protein kinase pathway, with dependence on activation of TGFBR-1 and apoptosis signal-regulating kinase 1.

EGFR/HER2 inhibitors effectively reduce the malignant potential of MDR breast cancer evoked by P-gp substrates in vitro and in vivo.

Multidrug resistance (MDR) induced by chemotherapy in breast cancer frequently leads to tumor invasion, metastasis and poor clinical outcome. We preliminarily found that the epidermal growth factor receptor (EGFR) is involved in enhancing the malignant potential of MDR breast cancer cells, but the mechanism remains unclear. In the present study, we demonstrated in vitro and in vivo that EGFR/HER2 promote the invasive and metastatic abilities of MDR breast cancer. More importantly, a new function of EGFR/HER2 inhibitors was revealed for the first time, which could improve the treatment efficacy of breast cancer by reversing the MDR process rather than by inhibiting tumor growth. Firstly, using quantitative real­time PCR and western blot analysis, we found that overexpression of EGFR/HER2 in MCF7/Adr cells upregulated CD147 and MMP2/9 at both the transcription and protein expression levels, which promoted tumor cell migration, as determined using an in vitro invasion assay. Secondly, the upregulated levels of CD147 and MMP2/9 were decreased when EGFR/HER2 activity was inhibited, and therefore tumor invasion was also significantly inhibited. These phenomena were also demonstrated in nude mouse assays. Additionally, in MDR breast cancer patients, we found that overexpression of EGFR and P­gp levels led to shorter overall survival (OS) and disease­free survival (DFS) by IHC assays and Kaplan­Meier survival analysis. In conclusion, EGFR/HER2 play a crucial role in enhancing CD147 and MMP expression to establish favorable conditions for invasion/metastasis in MDR breast cancer. The scope of application of EGFR/HER2 inhibitors may be expanded in EGFR/HER2­positive patients. We suggest that MDR breast cancer patients may benefit from novel therapies targeting EGFR/HER2.

CA IX is upregulated in CoCl2-induced hypoxia and associated with cell invasive potential and a poor prognosis of breast cancer.

Hypoxia, a common phenomenon during the development of malignant solid tumors including breast cancer, serves to propagate a cascade of molecular pathways triggered by hypoxia-inducible factor-1α (HIF-1α). Carbonic anhydrase IX (CA IX), one of the target genes of HIF-1α, has been reported to be involved in progression of malignant tumors. The objective of this study was to investigate the expression of HIF-1α and CA IX in hypoxia, involvement of CA IX in the regulation of migration and invasion/metastasis and its prognostic significance in breast cancer. We used cobalt chloride (CoCl2) as a hypoxia-mimetic agent and found that the expression of HIF-1α protein, CA IX mRNA and protein, is effectively upregulated, except for HIF-1α mRNA. Data showed that the elevated CA IX expression is closely related to in vitro cell migration and invasion, and the underlying mechanism of this process may be associated with epithelial-mesenchymal transition (EMT). The study of clinical tissue samples also demonstrated that CA IX is an independent prognostic marker that may serve as a useful clinical biomarker for predicting tumor progression and the invasion/metastasis of breast cancer. These results provide further insight into the role of CA IX in tumor progression and put forward further strong evidence as well as new consideration for CA IX target therapy.

UCH-L1 involved in regulating the degradation of EGFR and promoting malignant properties in drug-resistant breast cancer.

Ubiquitin carboxy terminal hydrolase-L1 (UCHL1) belongs to the UCH proteases family that deubiquitinates ubiquitin-protein conjugates in the ubiquitin-proteasome system. Our previous research showed that UCH-L1 and EGFR could regulate the expression of P-gp, CD147 and MMPs in multi-drug resistance (MDR) breast cancer cells, respectively. But it is still unclear whether direct regulation exists between the UCH-L1 and EGFR in MDR breast cancer. In order to clarify this, MDR human breast carcinoma cell line MCF7/Adr, that expresses relatively high UCH-L1, and its parental cell line MCF7, that expresses relatively low UCH-L1, were chosen for this study. We added ubiquitin proteasome inhibitor MG-132 into the culture of MCF7/Adr cells and transfected pIRES2-UCH-L1-EGFP plasmid into MCF7 cells, respectively. Using quantitative real-time polymerase chain reaction and western blot analyses, we found accompanying over-expression of UCH-L1, EGFR was up-regulated in both MCF7/ADR and MCF7 cells. Preliminary results indicated the degradation of EGFR might be regulated by ubiquitin level. So we speculated that up-regulated UCH-L1 could promote expression level of EGFR, thereby enhance the invasion and metastasis abilities of tumor cells. Moreover, to further explore the role of UCH-L1 and EGFR, we investigated the expression of UCH-L1, EGFR and P-gp in 65 local advanced breast cancer cases by immunohistochemistry assay. The result showed that the patients not responding to chemotherapy had higher UCH-L1, EGFR and P-gp expression levels and more lymph nodes metastasis. The Kaplan-Meier survival analysis showed that the patients with elevated UCH-L1 expression after chemotherapy presented shorter overall survival and disease free survival times than those with down-regulated or unchanged expression of UCH-L1. Our findings suggest that UCH-L1 may be an indicator of chemotherapy-response and poor-survival in breast cancer. UCH-L1 might be an appropriate target for improving chemo-resistant breast cancer therapy.

miR-320a is an independent prognostic biomarker for invasive breast cancer.

Breast cancer is one of the most common malignancies worldwide and is the second leading cause of cancer-related mortality among females. miRNAs are a class of small noncoding RNAs that are aberrantly expressed in human cancers. Due to their small size and stability, miRNAs have the potential to be efficacious clinical targets. MicroRNA-320a (miR-320a) has been shown to be dysregulated in multiple malignancies. In the present study, the expression levels of miR-320a were investigated in 15 paraffin-embedded in situ breast carcinoma and 130 invasive breast cancer tissues, and the prognostic value for breast cancer patients was assessed. Chromogenic in situ hybridization revealed that 60/130 (46%) invasive breast cancer tissues exhibited high expression levels of miR-320a (staining index score of ≥4). Furthermore, miR-320a staining was found to significantly correlate with tumor size (P=0.046), clinical stage (P<0.001), lymph node metastasis (P<0.001) and distant metastasis (P=0.006). In addition, patients exhibiting low miR-320a expression levels had shorter overall survival times (P<0.001). Univariate and multivariate analyses revealed that miR-320a was an independent prognostic biomarker for invasive breast cancer (hazard ratio, 0.221; 95% confidence interval, 0.050-0.979; P=0.047). Receiver operator characteristic curves revealed that the prognostic value of miR-320a was enhanced when compared with the widely used prognostic biomarkers (estrogen receptor, progesterone receptor and human epidermal growth factor-2) in invasive breast cancer. The results of the present study suggest that miR-320a presents a potential biomarker for the prognosis of invasive breast cancer, and dysregulation of miR-320a may be involved in invasive breast cancer progression.