Stem cell transplantation is a promising treatment for repairing damaged tissues, but challenges like immune rejection and ethical concerns remain. Mesenchymal stem cells (MSCs) offer high differentiation potential and immune regulatory activity, showing promise in treating diseases such as gynecological, neurological, and kidney disorders. With scientific progress, MSC applications are overcoming traditional treatment limitations. In MSCs-macrophage coculture, MSCs transform macrophages into anti-inflammatory M2 macrophages, reducing inflammation, whereas macrophages enhance MSCs osteogenic differentiation. This coculture is vital for immune modulation and tissue repair, with models varying by contact type and dimensional arrangements. Factors such as coculture techniques and cell ratios influence outcomes. Benefits include improved heart function, wound healing, reduced lung inflammation, and accelerated bone repair. Challenges include optimizing coculture conditions. This study reviews the methodologies, factors, and mechanisms of MSC-macrophage coculture, providing a foundation for tissue engineering applications. SIGNIFICANCE STATEMENT: This review underlines the significant role of mesenchymal stem cell-macrophage coculture, providing a foundation for tissue engineering application.

Following the publication of the above article, an interested reader drew the authors' attention to the fact that certain features shown in Fig. 6B, illustrating the tumors extracted from the animal in vivo experiments, were strikingly similar to images that had appeared in other papers by different authors published at around the same time. The authors conceded that the in vivo experiments reported in this study had been performed by a third party. Therefore, in the interests of preserving accuracy in the scientific record, the authors requested that this paper be retracted from the Journal. The Editor is in agreement that the paper should be retracted. All authors agree with the retraction of this article, and the Editor apologizes to the readership for any inconvenience caused. [the original article was published in Oncology Reports 45: 1094‑1104, 2021; DOI: 10.3892/or.2020.7908].

BACKGROUND:LINC00152 plays a crucial role in tumorigenesis and progression of multiple types of cancer. However, the biological significance of LINC00152 and its potential role in oral squamous cell carcinoma (OSCC) remain to be determined. In the present study, we investigated the role of LINC00152 and the underlying mechanism of its oncogenic activity in OSCC.MATERIALS AND METHODS:The expression of LINC00152 in OSCC tissues and cell lines was detected using qRT-PCR. Cell proliferation, colony formation, migration, and invasion were measured using a cell counting kit, colony formation assay, wound healing, and transwell invasion assays, respectively. The target gene of LINC00152 was confirmed using a dual-luciferase reporter assay and qRT-PCR. A nude mouse model was established to analyze the function of LINC00152 in vivo.RESULTS:LINC00152 expression was significantly upregulated in OSCC tissues and cell lines compared with that in normal counterparts. Upregulated LINC00152 served as an independent prognostic predictor in patients with OSCC. Moreover, knockdown of LINC00152 inhibited cell proliferation, colony formation, migration, and invasion, and suppressed the epithelial to mesenchymal transition in vitro, as well as impairing tumor growth in vivo. A mechanistic investigation indicated that LINC00152 could directly bind to miR-139-5p in OSCC. LINC00152 expression was inversely correlated with miR-139 expression in OSCC tissues.CONCLUSION:Taken together, these results suggested that LINC00152 may function as oncogene in OSCC and could be a potential therapeutic target in patients with OSCC.

Long non-coding RNA (lncRNA) actin filament-associated protein 1 antisense RNA 1 (AFAP1-AS1) has been reported to serve important roles in multiple types of cancer. However, the biological function and underlying mechanism of AFAP1-AS1 in oral squamous cell carcinoma (OSCC) remain largely unknown. The present study aimed to investigate the biological roles and clarify the potential mechanism of AFAP1-AS1 in OSCC. The expression levels of AFAP1-AS1 in OSCC tissues and cells were determined using reverse transcription-quantitative PCR. Cell proliferation, colony formation, migration and invasion were analyzed using Cell Counting Kit-8, colony formation, wound healing and Transwell invasion assays, respectively. The potential binding between AFAP1-AS1 and microRNA (miR)-145 was validated using dual luciferase reporter and RNA pull-down assays. A xenograft tumor model was established to evaluate the effect of AFAP1-AS1 in vivo. The results revealed that AFAP1-AS1 expression levels were markedly upregulated in OSCC tissues and cells. In addition, patients with OSCC with high expression levels of AFAP1-AS1 had a poor prognosis. Functionally, the knockdown of AFAP1-AS1 in OSCC cells significantly inhibited cell proliferation, migration and invasion in vitro. Similarly, in vivo AFAP1-AS1 knockdown prevented tumor growth and reduced tumor size and weight. Mechanistically, AFAP1-AS1 was discovered to regulate the expression levels of Homeobox A1 (HOXA1) by competing with miR-145. The inhibition of miR-145 partially attenuated the inhibitory effects of AFAP1-AS1 knockdown on OSCC cells. In conclusion, the findings of the present study suggested that AFAP1-AS1 may promote the progression of OSCC by regulating the miR-145/HOXA1 axis.

Opa-interacting protein 5 antisense RNA 1 (OIP5-AS1), a novel identified long noncoding RNA (lncRNA), has been suggested to serve as oncogene in multiple cancers. However, the functional involvement of OIP5-AS1 in oral squamous cell carcinoma (OSCC) was still unknown. The aims of this study were to investigate the functional role of OIP5-AS1 in OSCC and explore its potential mechanism. We found that OIP5-AS1 was up-regulated in OSCC tissues compared with adjacent non-tumor tissues. Loss-of-function experiments revealed that OIP5-AS1 knockdown significantly inhibited OSCC cell proliferation, migration and invasion in vitro, and retarded tumor growth in vivo. Mechanistically, OIP5-AS1 serves as a competing endogenous RNA of miR-338-3p and modulates the expression of neuropilin1 (NRP1), which has been identified as a downstream target gene of miR-338-3p in OSCC. Moreover, downregulation of miR-338-3p or overexpression of NRP1 partly reversed the inhibitory effect of OIP5-AS1 depletion on cell proliferation, migration and invasion. The current results provide evidences for the role of OIP5-AS1 in promoting OSCC progression by regulating miR-338-3p/NRP1 axis and suggest OIP5-AS1 as a potential therapy target for OSCC.

IntroductionReports suggest that lncRNAs have implications in the development of several diseases including cancer. It is therefore believed that lncRNAs may act as therapeutic targets for cancer treatment. The treatment of ovarian cancer is mainly obstructed by lack of biomarkers and efficient drug targets. Against this backdrop, this study was undertaken to reveal the role and therapeutic implications of lncRNA CCAT2 in ovarian cancer.Material and methodsExpression analysis was carried out with quantitative real-time polymerase chain reaction (qRT-PCR). Transfections were carried out using Lipofectamine 2000 reagent. Cell counting kit 8 (CCK-8) assays were used to determine the cell viability. AO/EB and annexin V/propidium iodide (PI) were used for detection of apoptosis. Wound healing and transwell assays were used to determine cell migration and invasion. The expression of the proteins was estimated by western blotting.ResultsThe results showed that the expression of CCAT2 was significantly overexpressed in ovarian cancer tissues and cell lines. Si-RNA mediated silencing of CCAT2 resulted in the decrease of proliferation rate and colony formation potential of the OVACAR-3 cells via induction of apoptotic cell death, which was also accompanied by cleavage of PARP, downregulation of Bcl-2 and upregulation of Bax, caspase-3 and caspase-9. Suppression of CCAT2 enhanced the chemosensitivity of the OVACAR-3 cells to cisplatin and also decreased their migration and invasion.ConclusionsThe findings of this study revealed that lncRNA CCAT2 suppression inhibits the proliferation, drug sensitivity, and metastasis of ovarian cancer and may prove beneficial in ovarian cancer management.

A bone morphogenetic protein-2(BMP-2) derived synthetic oligopeptide, S[PO4]KIPKASSVPTELSAI-STLYLDDD(P24), has shown great potential for facilitating bone regeneration. However, P24 cannot be directly used onto bone defects, while a continuous sustained delivery of P24 may lead to a better formation of bone tissue. Based on this issue, we have developed a sustained delivery system incorporating P24-loaded poly(lactide-co-glycolide) (PLGA) microspheres and nano-hydroxyapatite(n-HA) into the composite hydrogel. The P24-contained compound material was characterized with NMR, FTIR and SEM to demonstrate the formation of compound structure containing P24, PLGA and n-HA. A continuous drug release of P24 was observed for over 60 d that evidently enhanced the efficiency in promoting the proliferation of MC3T3-E1 cells and the secrete of alkaline phosphatase(ALP) in vitro. Moreover, the osteoinduction effect of the hydrogel system with P24 peptide microspheres was demonstrated in vivo and manifested by the result of immunohistochemistry. This novel injectable composite hydrogel is expected to be applied to improving the bone defect treatment in bone tissue engineering.

significance of LINC00152 and its potential role in oral squamous cell carcinoma (OSCC) remain to be determined. In the present study, we investigated the role of LINC00152 and the underlying mechanism of its oncogenic activity in OSCC. Materials and methods: The expression of LINC00152 in OSCC tissues and cell lines was detected using qRT-PCR. Cell proliferation, colony formation, migration, and invasion were measured using a cell counting kit, colony formation assay, wound healing, and transwell invasion assays, respectively. The target gene of LINC00152 was confirmed using a dual-luciferase reporter assay and qRT-PCR. A nude mouse model was established to analyze the function of LINC00152 in vivo. Results: LINC00152 expression was significantly upregulated in OSCC tissues and cell lines compared with that in normal counterparts. Upregulated LINC00152 served as an independent prognostic predictor in patients with OSCC. Moreover, knockdown of LINC00152 inhibited cell proliferation, colony formation, migration, and invasion, and suppressed the epithelial to mesenchymal transition in vitro, as well as impairing tumor growth in vivo. A mechanistic investigation indicated that LINC00152 could directly bind to miR-139-5p in OSCC. LINC00152 expression was inversely correlated with miR-139 expression in OSCC tissues. Conclusion: Taken together, these results suggested that LINC00152 may function as oncogene in OSCC and could be a potential therapeutic target in patients with OSCC.

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