Comprehensive Bibliometric Analysis of Stem Cell Research in Alzheimer's Disease from 2004 to 2022.

INTRODUCTION: Stem cell-based regenerative medicine has provided an excellent opportunity to investigate therapeutic strategies and innovative treatments for Alzheimer's disease (AD). However, there is an absence of visual overviews to assess the published literature systematically. METHODS: In this review, the bibliometric approach was used to estimate the searched data on stem cell research in AD from 2004 to 2022, and we also utilized CiteSpace and VOSviewer software to evaluate the contributions and co-occurrence relationships of different countries/regions, institutes, journals, and authors as well as to discover research hot spots and encouraging future trends in this field. RESULTS: From 2004 to 2022, a total of 3,428 publications were retrieved. The number of publications and citations on stem cell research in AD has increased dramatically in the last nearly 20 years, especially since 2016. North America and Asia were the top 2 highest output regions. The leading country in terms of publications and access to collaborative networks was the USA. Centrality analysis revealed that the UCL (0.05) was at the core of the network. The Journal of Alzheimer's Disease (n = 102, 2.98%) was the most productive academic journal. The analyses of keyword burst detection indicated that exosomes, risk factors, and drug delivery only had burst recently. Citations and co-citation achievements clarified that cluster #0 induced pluripotent stem cells, #2 mesenchymal stem cells, #3 microglia, and #6 adult hippocampal neurogenesis persisted to recent time. CONCLUSION: This bibliometric analysis provides a comprehensive guide for clinicians and scholars working in this field. These analysis and results hope to provide useful information and references for future understanding of the challenges behind translating underlying stem cell biology into novel clinical therapeutic potential in AD.

Over 400 W graded-index fiber Raman laser with brightness enhancement.

The power scaling on all-fiberized Raman fiber oscillator with brightness enhancement (BE) based on multimode graded-index (GRIN) fiber is demonstrated. Thanks to beam cleanup of GRIN fiber itself and single-mode selection properties of the fiber Bragg gratings inscribed in the center of GRIN fiber, the efficient BE is realized. For the laser cavity with single OC FBG, continuous-wave power of 334 W with an M2 value of 2.8 and BE value of 5.6 were obtained at a wavelength of 1120 nm with an optical-to-optical efficiency of 49.6%. Furthermore, the cavity reflectivity is increased by employing two OC FBGs to scale the output power up to 443 W, while the corresponding M2 is 3.5 with BE of 4.2. To our best knowledge, it is the highest power in Raman oscillator based on GRIN fiber.

Kilowatt level Raman amplifier based on 100 µm core diameter multimode GRIN fiber with M2 = 1.6.

In this Letter, we demonstrate a high-power Raman fiber amplifier with excellent beam quality based on graded-index fiber. The Yb-doped fiber laser (YDFL) and bandwidth-tunable amplified spontaneous emission (ASE) source are employed as the pump source to compare the laser performance separately. When the ASE with a bandwidth of 8 nm is employed, a maximum power of 943 W at 1130 nm is achieved, which is twice that pumped by YDFL. The beam quality factor M2 at maximum output power is 1.6, with a brightness enhancement (BE) factor of 27. To the best of our knowledge, this is the best beam quality and BE factor based on pure Raman gain with output power of over 100 W.

Brightness enhancement in random Raman fiber laser based on a graded-index fiber with high-power multimode pumping.

A brightness-enhanced random Raman fiber laser (RRFL) with maximum power of 306 W at 1120 nm is demonstrated. A half-open cavity is built based on a graded-index (GRIN) passive fiber and single high-reflective fiber Bragg grating written in it directly. Due to the beam cleanup effect in the GRIN fiber enhanced in the half-open RRFL cavity, the output beam quality factor M2 is improved from 9.15 (pump) to 1.76-2.35 (Stokes) depending on power, while the pump-Stokes brightness enhancement (BE) factor increases proportionally to output power reaching 6.1 at maximum. To the best of our knowledge, this is the highest power GRIN RRFL with BE.

Risk factors for secondary hemophagocytic lymphohistiocytosis in severe coronavirus disease 2019 adult patients.

BACKGROUND: Secondary hemophagocytic lymphohistiocytosis (sHLH) is a life-threatening hyperinflammatory event and a fatal complication of viral infections. Whether sHLH may also be observed in patients with a cytokine storm induced by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection is still uncertain. We aimed to determine the incidence of sHLH in severe COVID-19 patients and evaluate the underlying risk factors. METHOD: Four hundred fifteen severe COVID-19 adult patients were retrospectively assessed for hemophagocytosis score (HScore). A subset of 7 patients were unable to be conclusively scored due to insufficient patient data. RESULTS: In 408 patients, 41 (10.04%) had an HScore ≥169 and were characterized as "suspected sHLH positive". Compared with patients below a HScore threshold of 98, the suspected sHLH positive group had higher D-dimer, total bilirubin, alanine aminotransferase, aspartate aminotransferase, blood urea nitrogen, serum creatinine, triglycerides, ferritin, interleukin-6, C-reactive protein, procalcitonin, lactate dehydrogenase, creatine kinase isoenzyme, troponin, Sequential Organ Failure Assessment (SOFA) score, while leukocyte, hemoglobin, platelets, lymphocyte, fibrinogen, pre-albumin, albumin levels were significantly lower (all P < 0.05). Multivariable logistic regression revealed that high ferritin (>1922.58 ng/mL), low platelets (<101 × 109/L) and high triglycerides (>2.28 mmol/L) were independent risk factors for suspected sHLH in COVID-19 patients. Importantly, COVID-19 patients that were suspected sHLH positive had significantly more multi-organ failure. Additionally, a high HScore (>98) was an independent predictor for mortality in COVID-19. CONCLUSIONS: HScore should be measured as a prognostic biomarker in COVID-19 patients. In particular, it is important that HScore is assessed in patients with high ferritin, triglycerides and low platelets to improve the detection of suspected sHLH.

Down-regulation of circDMNT3B is conducive to intestinal mucosal permeability dysfunction of rats with sepsis via sponging miR-20b-5p.

Sepsis is a life-threatening syndrome with a high risk of mortality, which is caused by the dysregulated host response to infection. We examined significant roles of circDMNT3B and miR-20b-5p in the intestinal mucosal permeability dysfunction of rats with sepsis. SD rats were randomly divided into 6 groups (n = 10/group): sham group, sepsis group, si-negative control group, circDNMT3B-si1 group, circDNMT3B-si2 group and circDNMT3B-si1 + anti-miR-20b-5p group. The level of malondialdehyde (MDA) content, superoxide dismutase (SOD) activity, interleukin (IL)-6 and IL-10 levels were measured through ELISA assay kits. Cell survival rate and cell apoptosis were evaluated by Cell-Counting Kit-8 Assay and flow cytometry, respectively. Luciferase reporter assays were used to investigate interactions between miR-20b-5p circDMNT3B in HEK-293T cells. Silencing circDNMT3B can significantly increase the level of d-lactic acid, FD-40, MDA, diamine oxidase, IL-10 and IL-6, compared with sepsis group, while the SOD activity was lower. Silencing circDNMT3B leads to oxidative damage and influence inflammatory factors level in intestinal tissue. CircDNMT3B was identified as a target gene of miR-20b-5p. Silencing circDNMT3B decreased cell survival and induced apoptosis in Caco2 cells treated with LPS, which was reversed by anti-miR-20b-5p. MiR-20b-5p inhibitor remarkably down-regulated mentioned-above levels, in addition to up-regulate SOD activity, which may relieve the damage of intestinal mucosal permeability caused by silencing circDNMT3B in sepsis rats. Down-regulation of circDMNT3B was conducive to the dysfunction of intestinal mucosal permeability via sponging miR-20b-5p in sepsis rats, which may provide the novel strategy for sepsis treatment in the future.

2†kW high-efficiency Raman fiber amplifier based on passive fiber with dynamic analysis on beam cleanup and fluctuation.

In this paper, we study the power scaling in high power continuous-wave Raman fiber amplifier employing graded-index passive fiber. The maximum output power reaches 2.087 kW at 1130 nm with an optical conversion efficiency of 90.1% (the output signal power versus the depleted pump power). To the best of our knowledge, this is the highest power in the fields of Raman fiber lasers based merely on Stokes radiation. The beam quality parameter M2 improves from 15 to 8.9 during the power boosting process, then beam spot distortion appears at high power level. This is the first observation and analysis on erratic dynamic properties of the transverse modes in high power Raman fiber amplifier.

Power scaling of Raman fiber amplifier based on the optimization of temporal and spectral characteristics.

We comprehensively study the effects of temporal and spectral optimization on single-mode Raman fiber amplifiers. Amplified spontaneous emission sources and ytterbium-doped fiber lasers are employed as seed or pump lasers for comparison, and passive fibers are utilized as gain media. The influences of various parameters of the laser on 2nd order Raman threshold and maximum output power are investigated experimentally, including bandwidth, seed power, wavelength separation between pump and seed laser, and temporal stability. With the 190 m passive fiber, the output power increases from 99.5 W to 142.4 W, corresponding to 43.1% improvement through the optimization of seed laser power, pump wavelength and temporal performance of pump source in this amplifier, which has guidance on the establishment of high-power single-mode Raman fiber amplifiers.

High-power cladding pumped Raman fiber amplifier with a record beam quality.

In this Letter, a high-power, high-brightness all-fiberized Raman amplifier based on a cladding-pumping scheme is presented for the first time, to the best of our knowledge. The triple-clad passive fiber is employed as Raman gain fiber in the laser system. The maximum output power is 762.6 W emitting at 1130 nm. To the best of our knowledge, this is the highest power in the fields of cladding-pumped Raman amplifiers. Through a cladding-pumping process, the beam quality parameter ${{\rm M}^2}$M2 improves from 6.12 of seed laser to 2.24 at maximum output power of 762.6 W, while the best ${{\rm M}^2}$M2 is 1.9 at 267.2 W. It is also the best beam quality of Raman laser with brightness enhancement in any kind of configuration (graded-index fiber or multi-clad fiber, laser or amplifier, all-fiber or free-space configuration) with power of over 100 W.

All-fiberized cascaded random Raman fiber laser with high spectral purity based on filtering feedback.

Cascaded random Raman fiber lasers (CRRFLs) with simple configuration and high spectral purity have become a great candidate for power scaling over the 1.1 µm-2 µm spectral band. Recently, CRRFLs with high spectral purity over 90% have been proposed by applying a highly temporal-stable pump source or a free-space short-pass filter, at the cost of increased system complexity. In this work, pumped directly by a Yb-doped fiber oscillator at 1080 nm, an all-fiberized and simplified CRRFL with a short-pass optical filter based on bending fiber and a thin-film wavelength division multiplexer is demonstrated. The transmission loss of the filter for 5th Stokes order at 1440 nm is up to 70 dB. Spectral purity over 92% for all the first four Stokes orders is achieved. The highest output power is 15 W for the 4th Stokes order at 1341 nm.

Nucleus of Circulating Tumor Cell Determines Its Translocation Through Biomimetic Microconstrictions and Its Physical Enrichment by Microfiltration.

The mechanism of cells passing through microconstrictions, such as capillaries and endothelial junctions, influences metastasis of circulating tumor cells (CTCs) in vivo, as well as size-based enrichment of CTCs in vitro. However, very few studies observe such translocation of microconstrictions in real time, and thus the inherent biophysical mechanism is poorly understood. In this study, a multiplexed microfluidic device is fabricated for real-time tracking of cell translocation under physiological pressure and recording deformation of the whole cell and nucleus, respectively. It is found that the deformability and size of the nucleus instead of the whole cell dominate cellular translocation through microconstrictions under a normal physiological pressure range. More specifically, cells with a large and stiff nucleus are prone to be blocked by relatively small constrictions. The same phenomenon is also observed in the size-based enrichment of CTCs from peripheral blood of metastatic cancer patients. These findings are different from a popular viewpoint that the size and deformability of a whole cell mainly determine cell translation through microconstrictions, and thus may elucidate interactions between CTCs and capillaries from a new perspective and guide the rational design of size-based microfilters for rare cell enrichment.

Label-Free Virus Capture and Release by a Microfluidic Device Integrated with Porous Silicon Nanowire Forest.

Viral diseases are perpetual threats to human and animal health. Detection and characterization of viral pathogens require accurate, sensitive, and rapid diagnostic assays. For field and clinical samples, the sample preparation procedures limit the ultimate performance and utility of the overall virus diagnostic protocols. This study presents the development of a microfluidic device embedded with porous silicon nanowire (pSiNW) forest for label-free size-based point-of-care virus capture in a continuous curved flow design. The pSiNW forests with specific interwire spacing are synthesized in situ on both bottom and sidewalls of the microchannels in a batch process. With the enhancement effect of Dean flow, this study demonstrates that about 50% H5N2 avian influenza viruses are physically trapped without device clogging. A unique feature of the device is that captured viruses can be released by inducing self-degradation of the pSiNWs in physiological aqueous environment. About 60% of captured viruses can be released within 24 h for virus culture, subsequent molecular diagnosis, and other virus characterization and analyses. This device performs viable, unbiased, and label-free virus isolation and release. It has great potentials for virus discovery, virus isolation and culture, functional studies of virus pathogenicity, transmission, drug screening, and vaccine development.

Atractylodes lactone compounds inhibit platelet activation.

Platelets play a crucial role in the development and progression of atherosclerosis-thrombosis and, therefore, antiplatelet drugs are widely used in the treatment of coronary artery disease. Moreover, advances in understanding the biological functions of natural plant products can provide new pharmacological strategies aimed at promoting cardiovascular health. Atractylenolide I (ATL-1), ATL-2, and ATL-3 are the major bioactive components of a Qi tonifying medicinal herb Rhizoma Atractylodis Macrocephalae (Atractylodes macrocephala), which is commonly used in traditional Chinese medicine (TCM). These components possess well-documented anti-inflammatory and anticancer activities, but their effects on platelet activation are still unknown. In this study, the effects of ATL on platelet function in vitro and in vivo were investigated, and the underlying mechanism was explored. We found that ATL-2 and ATL-3 but not ATL-1 diminished agonist-induced platelet aggregation and diminished adenosine triphosphate (ATP) release from dense granules. The levels of phospho-Akt (Ser473) and phospho-p38 MAPK were downregulated in the presence of ATL-2 and ATL-3. We also found that ATL-2 and ATL-3 have a similar inhibitory effect on platelet activation as acetylsalicylic acid in response to agonists. Furthermore, ATL-2 and ATL-3 diminished the spreading of human platelets on immobilized fibrinogen (Fg), delayed clot retraction in platelet-depleted plasma containing human platelets, extended first occlusion time in a mouse model of ferric chloride (FeCl3)-induced carotid arterial thrombosis, and prolonged the bleeding time. These observations suggest that ATL-2 and ATL-3 are potential candidate therapeutic drugs for the prevention of thrombosis.

Role of Myoendothelial Gap Junctions in the Regulation of Human Coronary Artery Smooth Muscle Cell Differentiation by Laminar Shear Stress.

BACKGROUND/AIMS: Smooth muscle cells may dedifferentiate into the synthetic phenotype and promote atherosclerosis. Here, we explored the role of myoendothelial gap junctions in phenotypic switching of human coronary artery smooth muscle cells (HCASMCs) co-cultured with human coronary artery endothelial cells (HCAECs) exposed to shear stress. METHODS: HCASMCs and HCAECs were seeded on opposite sides of Transwell inserts, and HCAECs were exposed to laminar shear stress of 12 dyn/cm2 or 5 dyn/cm2. The myoendothelial gap junctions were evaluated by using a multi-photon microscope. RESULTS: In co-culture with HCAECs, HCASMCs exhibited a contractile phenotype, and maintained the expression of differentiation markers MHC and H1-calponin. HCASMCs and HCAECs formed functional intercellular junctions, as evidenced by colocalization of connexin(Cx)40 and Cx43 on cellular projections inside the Transwell membrane and biocytin transfer from HCAECs to HCASMCs. Cx40 siRNA and 18-α-GA attenuated protein expression of MHC and H1-calponin in HCASMCs. Shear stress of 5 dyn/cm2 increased Cx43 and decreased Cx40 expression in HCAECs, and partly inhibited biocytin transfer from HCAECs to HCASMCs, which could be completely blocked by Cx43 siRNA or restored by Cx40 DNA transfected into HCAECs. The exposure of HCAECs to shear stress of 5 dyn/cm2 promoted HCASMC phenotypic switching, manifested by morphological changes, decrease in MHC and H1-calponin expression, and increase in platelet-derived growth factor (PDGF)-BB release, which was partly rescued by Cx43 siRNA or Cx40 DNA or PDGF receptor signaling inhibitor. CONCLUSIONS: The exposure of HCAECs to shear stress of 5 dyn/cm2 caused the dysfunction of Cx40/Cx43 heterotypic myoendothelial gap junctions, which may be replaced by homotypic Cx43/Cx43 channels, and induced HCASMC transition to the synthetic phenotype associated with the activation of PDGF receptor signaling, which may contribute to shear stress-associated arteriosclerosis.

Low-frequency shift Raman spectroscopy using atomic filters.

A Faraday anomalous dispersion optical filter (FADOF) and an atomic resonant absorption filter are used in tandem to demonstrate a low-frequency shift Raman measurement down to few cm-1. The FADOF, with an ultralow bandwidth of 0.08 cm-1 at 780 nm, serves as a bandpass filter, while the rubidium atomic cell acts as a notch filter which has a bandwidth of 0.3 cm-1. A proof-of-concept study to measure a Raman signal generated from a silica optical fiber is performed, demonstrating a low-frequency measurement of both the Stokes and the anti-Stokes shift down to 3 cm-1 at an equivalent signal level. These results indicate the prospect for gigahertz-terahertz low-energy Raman spectroscopy based on atomic filters.

Laser diode-pumped dual-cavity high-power fiber laser emitting at 1150 nm employing hybrid gain.

We demonstrate a laser diode-pumped dual-cavity high-power fiber laser emitting at 1150 nm. The laser employs Yb and Raman gains simultaneously. The fiber laser with a simple structure achieves high-efficiency operation while efficiently suppressing the amplified spontaneous emission and parasitic oscillation. The maximum output power at 1150 nm is 110.8 W, with an optical-to-optical efficiency of 57%. Further power scaling at 1150 nm is expected with the optimization of the system design.

Curcumin Modulates Macrophage Polarization Through the Inhibition of the Toll-Like Receptor 4 Expression and its Signaling Pathways.

BACKGROUND: Curcumin, the active ingredient in curcuma rhizomes, has a wide range of therapeutic effects. However, its atheroprotective activity in human acute monocytic leukemia THP-1 cells remains unclear. We investigated the activity and molecular mechanism of action of curcumin in polarized macrophages. METHODS: Phorbol myristate acetate (PMA)-treated THP-1 cells were differentiated to macrophages, which were further polarized to M1 cells by lipopolysaccharide (LPS; 1 µg/ml) and interferon (IFN)-γ (20 ng/ml) and treated with varying curcumin concentrations. [3H]thymidine (3H-TdR) incorporation assays were utilized to measure curcumin-induced growth inhibition. The expression of tumor necrosis factor-α (TNF-α), interleukin (IL-6), and IL-12B (p40) were measured by quantitative real-time polymerase chain reaction (PCR) and enzyme-linked immunosorbent assay (ELISA). Macrophage polarization and its mechanism were evaluated by flow cytometry and western blot. Additionally, toll-like receptor 4 (TLR4) small interfering RNA and mitogen-activated protein kinase (MAPK) inhibitors were used to further confirm the molecular mechanism of curcumin on macrophage polarization. RESULTS: Curcumin dose-dependently inhibited M1 macrophage polarization and the production of TNF-α, IL-6, and IL-12B (p40). It also decreased TLR4 expression, which regulates M1 macrophage polarization. Furthermore, curcumin significantly inhibited the phosphorylation of ERK, JNK, p38, and nuclear factor (NF)-κB. In contrast, SiTLR4 in combination with p-JNK, p-ERK, and p-p38 inhibition reduced the effect of curcumin on polarization. CONCLUSIONS: Curcumin can modulate macrophage polarization through TLR4-mediated signaling pathway inhibition, indicating that its effect on macrophage polarization is related to its anti-inflammatory and atheroprotective effects. Our data suggest that curcumin could be used as a therapeutic agent in atherosclerosis.

Manufacture and evaluation of nano-silver-poly-DL-lactide-co-caprolactone-small intestinal submucosa biological mesh in abdominal wall reconstruction.

Background: Inguinal hernia repair is a routine surgical procedure and many methods are being applied to improve the operation. In this study, an abdominal wall defect model was established in New Zealand rabbits. The safety and efficacy of the test product was evaluated by observing the physiological state and clinical manifestations and conducting anatomical observations in the rabbits after use of the nano-silver-poly-DL-lactide-co-caprolactone-small intestinal submucosa (NS-PLCL-SIS) mesh. Methods: A total of 18 New Zealand rabbits were randomly divided into a test group and a blank group. Routine blood and serum biochemical tests, and anatomical observations were conducted on postoperative day 30 (D30), day 60 (D60), and day 90 (D90). During the study period, all animals underwent clinical observation, and the obtained data were counted. Results: The results showed that the NS-PLCL-SIS mesh was degraded within 90 days, and there was no abnormal reaction and no animal death during the test. There was no significant difference in the changes of animal body weight at each time point. There was no infectious inflammatory reaction in the wound at the study site, and the ocular wound healed well 7 days after the operation. Conclusions: Under the conditions of this experiment, the NS-PLCL-SIS mesh had good performance in the repair of abdominal wall defect in New Zealand rabbits and is clinically safe for veterinarians.

Remimazolam attenuates myocardial ischemia-reperfusion injury by inhibiting the NF-ĸB pathway of macrophage inflammation.

BACKGROUND: Inflammation is a major contributing factor in myocardial ischemia/reperfusion (I/R) injury, and targeting macrophage inflammation is an effective strategy for myocardial I/R therapy. Though remimazolam is approved for sedation, induction, and the maintenance of general anesthesia in cardiac surgery, its effect on cardiac function during the perioperative period has not been reported. Therefore, this research aimed to explore the impact of remimazolam on inflammation during myocardial ischemia/reperfusion (I/R) injury. METHODS: An in vivo myocardial I/R mice model and an in vitro macrophage inflammation model were used to confirm remimazolam's cardiac protective effect. In vivo, we used echocardiography, hematoxylin and eosin (HE), and terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) staining to determine remimazolam's therapeutic effects on myocardial I/R injury and inflammation. In vitro, we employed enzyme-linked immunosorbent assay (ELISA), Western blot, Real-time Quantitative PCR (qPCR), flow cytometry, and immunofluorescence staining to assess inflammatory responses, especially remimazolam's effects on macrophage polarization after I/R. Furthermore, molecular docking was used to identify its potential binding targets on the inflammatory pathway to explore the mechanism of remimazolam. RESULTS: Remimazolam exhibited significant anti-myocardial I/R injury activity by inhibiting macrophage-mediated inflammation to reduce myocardial infarction, enhancing cardiac function. In addition, macrophage depletion counteracted improved cardiac function by remimazolam treatment. Mechanistically, the activated NF-ĸB signaling pathway and phosphorylation of p50 and p65 were repressed for anti-inflammatory effect. Consistently, two binding sites on p50 and p65 were identified by molecular docking to affect their phosphorylation of the Ser, Arg, Asp, and His residues, thus regulating NF-κB pathway activity. CONCLUSION: Our results unveil the therapeutic potential of remimazolam against myocardial I/R injury by inhibiting macrophages polarizing into the M1 type, alleviating inflammation.

Tumor-derived mesenchymal progenitor cell-related genes in the regulation of breast cancer proliferation.

Background: Breast cancer (BC) is one of the most common malignancies worldwide, and its development is affected in various ways by the tumor microenvironment (TME). Tumor-derived mesenchymal progenitor cells (MPCs), as the most important components of the TME, participate in the proliferation and metastasis of BC in several ways. In this study, we aimed to characterize the genes associated with tumor-derived MPCs and determine their effects on BC cells. Methods: Tumor-derived MPCs and normal breast tissue-derived mesenchymal stem cells (MSCs) were isolated from tissues specimens of patients with BC. We conducted culture and passage, phenotype identification, proliferation and migration detection, inflammatory factor release detection, and other experiments on isolated MPCs from tumors and MSCs from normal breast tissues. Three paired tumor-derived MPCs and normal breast tissue-derived MSCs were then subjected to transcriptome analysis to determine the expression profiles of the relevant genes, and quantitative real-time polymerase chain reaction (qRT-PCR) was used to further confirm gene expression. Subsequently, the overexpression plasmids were transfected into tumor-derived MPCs, and the expression of various inflammatory factors of tumor-derived MPCs and their proliferation were characterized with a cell viability test reagent (Cell Counting Kit 8). Subsequently, the transfected tumor-derived MPCs were cocultured with BC cells using a conditioned medium coculture method to clarify the role of tumor-derived MSCs in BC. Results: Tumor-derived MPCs expressed stem cell characteristics including CD105, CD90, and CD73 and exhibited adipogenic and osteogenic differentiation in vitro. The proliferation of tumor-derived MPCs was significantly lower than that of normal breast tissue-derived MSCs, and the invasive metastatic ability was comparable; however, MPCs were found to release inflammatory factors such as interleukin 6 (IL-6) and transforming growth factor ß (TGF-ß). Transcriptome analysis showed that stomatin (STOM), collagen and calcium binding EGF domains 1 (CCBE1), and laminin subunit alpha 5 (LAMA5) were significantly upregulated in tumor-derived MPCs. Among them, STOM was highly expressed in tumor-derived MPCs, which mediated the slow proliferation of MPCs and promoted the proliferation of BC cells. Conclusions: STOM, CCBE1, and LAMA5 were highly expressed in tumor-derived MPCs, with STOM being found to retard the proliferation of MPCs but promote the proliferation of BC cells. There findings present new possibilities in targeted microenvironmental therapy for BC.