Effects of vibration training on upper limbs of volleyball players / Efeitos do treinamento vibratório sobre os membros superiores dos jogadores de voleibol / Efectos del entrenamiento con vibraciones en las extremidades superiores de los jugadores de voleibol

ABSTRACT Introduction: The research on vibration training has experienced a period of development in many projects, such as badminton, handball, long jump, and volleyball. However, there is still no quantitative research evaluation of its effects on the development of shoulder, elbow, and upper limb muscle strength in volleyball athletes. It is believed that a specific training protocol with vibration may bring benefits to sensory-motor performance and muscle strength implementation in volleyball athletes. Objective: To study the effects of vibration training on upper limb function in volleyball players. Methods: Literature, experimental, and mathematical-statistical research methods were used to explore the relationship between vibration training under the muscle strength of the upper limbs and their joints. Results: The vibration training with an amplitude of 2mm, at a vibration frequency between 30Hz and 45Hz, the frequency of vibration training presented inversely proportional to the effect of vibration training. Conclusion: Vibration training showed the benefits of motor coordination and increased muscle strength in volleyball players. An appropriate vibration training strategy can maximize athletes' skills, such as body coordination, flexibility, and jumping ability. Level of evidence II; Therapeutic studies - investigation of treatment outcomes.

RESUMO Introdução: A pesquisa sobre o treinamento por vibração experimentou um período de desenvolvimento sendo aplicada em muitos projetos como badminton, handebol, salto em distância e voleibol. Entretanto, ainda não há uma avaliação quantitativa da pesquisa sobre seus efeitos em ombro, cotovelo e sobre o desenvolvimento de força muscular nos membros superiores dos atletas de voleibol. Acredita-se que um protocolo de treino específico com vibração possa trazer benefícios ao desempenho sensório-motor e implementação de força muscular nos atletas de voleibol. Objetivo: Estudar os efeitos do treinamento por vibração sobre a função dos membros superiores dos jogadores de vôlei. Métodos: Utilizou-se métodos de pesquisa bibliográfica, experimental e estatística matemática para explorar a relação entre o treinamento vibratório sob a força muscular dos membros superiores e suas articulações. Resultados: O treinamento vibratório com amplitude de 2mm, numa frequência de vibração entre 30Hz e 45Hz, a frequência do treinamento vibratório apresentou-se inversamente proporcional ao efeito do treinamento vibratório. Conclusão: O treinamento vibratório mostrou benefícios de coordenação motora e aumento de força muscular nos jogadores de voleibol. Uma estratégia adequada de treinamento por vibração pode maximizar as habilidades dos atletas, tais como coordenação corporal, flexibilidade e habilidade de salto. Nível de evidência II; Estudos terapêuticos - investigação dos resultados do tratamento.

RESUMEN Introducción: La investigación sobre el entrenamiento con vibraciones ha experimentado un periodo de desarrollo aplicándose en muchos proyectos como el bádminton, el balonmano, el salto de longitud y el voleibol. Sin embargo, todavía no hay una evaluación cuantitativa de la investigación sobre sus efectos en el hombro, el codo y en el desarrollo de la fuerza muscular en las extremidades superiores de los atletas de voleibol. Se cree que un protocolo de entrenamiento específico con vibración puede aportar beneficios al rendimiento sensomotor y a la implementación de la fuerza muscular en los atletas de voleibol. Objetivo: Estudiar los efectos del entrenamiento con vibraciones sobre la función de las extremidades superiores en jugadores de voleibol. Métodos: Se utilizaron métodos de investigación literarios, experimentales y estadísticos matemáticos para explorar la relación entre el entrenamiento con vibración bajo la fuerza muscular de los miembros superiores y sus articulaciones. Resultados: El entrenamiento vibratorio con amplitud de 2mm, en una frecuencia de vibración entre 30Hz y 45Hz, la frecuencia del entrenamiento vibratorio se presentó inversamente proporcional al efecto del entrenamiento vibratorio. Conclusión: El entrenamiento con vibraciones mostró beneficios de coordinación motora y aumento de la fuerza muscular en jugadores de voleibol. Una estrategia adecuada de entrenamiento con vibraciones puede maximizar las habilidades de los atletas, como la coordinación corporal, la flexibilidad y la capacidad de salto. Nivel de evidencia II; Estudios terapéuticos - investigación de los resultados del tratamiento.

Smoke-induced SAV1 Gene Promoter Hypermethylation Disrupts YAP Negative Feedback and Promotes Malignant Progression of Non-small Cell Lung Cancer.

YAP (gene symbol YAP1) as a potential oncoprotein, is positively correlated with the malignancy of various tumors. However, overexpression of YAP alone in multiple normal tissue cells has failed to induce tumor formation and the underlying mechanism is poorly understood. Herein, we show that YAP activation directly induces transcription of its negative regulator, SAV1, to constitute a negative feedback loop, which plays a vital role in maintaining lung epithelial cell homeostasis and was dysregulated in non-small cell lung cancer (NSCLC). Notably, smoking promotes the hypermethylation of the SAV1 promoter region, which disrupts YAP negative feedback by inactivating the Hippo pathway. Besides, exogenous overexpression of SAV1 can act as a traffic protein, activating the Hippo signaling and concurrently inhibiting the WNT pathway to decrease cancer cell growth. Furthermore, using the lung cancer organoids, we found that lentivirus-mediated SAV1 gene transfer combined with methylation inhibitor and YAP-TEAD inhibitor is a potential feasible clinical medication regimen for the lung cancer patient, especially among the smoking population. Thus, this SAV1 mediated feedback loop provides an efficient mechanism to establish the robustness and homeostasis of YAP regulation and as a potential target of gene therapy for the smoking NSCLC population.

Citric acid-assisted phytoextraction of trace elements in composted municipal sludge by garden plants.

Sludge landscaping after compost stabilization is a popular recycling process; however, until trace elements (TEs) are extracted by plants and reduced to safe concentrations, they present a potential exposure risk. Three garden plants, Liriope platyphylla Wang et Tang (L. platyphylla), Iris tectorum Maxim (I. tectorum), and Photinia x fraseri Dress (P. x fraseri), were selected for field experiments, and their ability to phytoremediate TEs and the promotion effect of citric acid (CA) were studied over 3 months of observation. Among the three kinds of plants, L. platyphylla had the highest biomass per unit soil area, and the CA treatment further increased the biomass of this plant per unit soil area as well as the uptake of TEs. When treated with 3 mmol kg-1 CA, L. platyphylla showed increases in the bioconcentration factors of Cu, Zn, Pb, and Cd by 24%, 63%, 27%, and 123%, respectively. Because of the large biomass and high concentrations of TEs, L. platyphylla had high phytoremediation indexes for Zn, Cu, Pb, Ni, and Cd, which reached 18.5, 3.7, 3.2, 2.2, and 0.4 mg m-2, respectively, and were further improved by 60%-187% by the CA treatment. These advantages indicate the potential usefulness of L. platyphylla for phytoremediation. The results provide basic data and technical support for the use of sludge-based compost and phytoremediation by garden plants.

Downregulation of FOXO3a by DNMT1 promotes breast cancer stem cell properties and tumorigenesis.

Breast cancer stem cells (BCSCs) are tumor initiating cells that can self-renew and are highly tumorigenic and chemoresistant. Therefore, the identification of factors critical for BCSC function is vital for the development of therapies. Here, we report that DNMT1-mediated FOXO3a promoter hypermethylation leads to downregulation of FOXO3a expression in breast cancer. FOXO3a is functionally related to the inhibition of FOXM1/SOX2 signaling and to the consequent suppression of BCSCs properties and tumorigenicity. Moreover, we found that SOX2 directly transactivates DNMT1 expression and thereby alters the methylation landscape, which in turn feedback inhibits FOXO3a expression. Inhibition of DNMT activity suppressed tumor growth via regulation of FOXO3a/FOXM1/SOX2 signaling in breast cancer. Clinically, we observed a significant inverse correlation between FOXO3a and FOXM1/SOX2/DNMT1 expression levels, and loss of FOXO3a expression or increased expression of FOXM1, SOX2, and DNMT1 predicted poor prognosis in breast cancer. Collectively, our findings suggest an important role of the DNMT1/FOXO3a/FOXM1/SOX2 pathway in regulating BCSCs properties, suggesting potential therapeutic targets for breast cancer.

Cip2a/miR-301a feedback loop promotes cell proliferation and invasion of triple-negative breast cancer.

Triple-negative breast cancer (TNBC) is a highly aggressive breast cancer subtype and lacks effective targeted therapies. Cancerous inhibitor of protein phosphatase 2A (Cip2a) is an oncogene that is known to inhibit PP2A tumor suppressor activity in human malignancies. We previously demonstrated that Cip2a is a novel target for the treatment of TNBC. However, the functional roles of Cip2a in TNBC progression are still not fully characterized. In this study, we identified that miR-301a is a novel target of Cip2a in TNBC cell lines by miRNA microarray analysis. We found that Cip2a increases E2F1 expression, which in turn transcriptional activates miR-301a by occupying the miR-301a host gene SKA2 promoter. Moreover, we found that miR-301a level is significantly increased in TNBC tissues, and up-regulation of miR-301a is responsible for Cip2a-induced cell proliferation and invasion of TNBC cells. Furthermore, miR-301a feedback promotes the expression of Cip2a via activation of ERK/CREB signaling. Together, our study suggests an auto-regulatory feedback loop between Cip2a and miR-301a and this auto-regulatory loop might play an important role in TNBC progression.

Activation of FOXO3a reverses 5-Fluorouracil resistance in human breast cancer cells.

Breast cancer is the most frequently diagnosed tumor type and the primary leading cause of cancer deaths in women worldwide. Drug resistance is the major obstacle for breast cancer treatment improvement. TRAIL-inducing compound 10 (Tic10), a novel activator of FOXO3, exhibits potent antitumor efficacy both in vitro and in vivo. In the present study, we investigated the resistance reversal effect of Tic10 on multidrug-resistant breast cancer cells T47D/5Fu derived from T47D breast cancer cells. We found that FOXO3a was significantly decreased in T47D/5-Fu cells, whereas treatment of Tic10 enhances FOXO3a expression and nuclear translocation. Moreover, treatment of Tic10 could reverses 5-Fluorouracil resistance of T47D/5-Fu cells via induction of G0/G1 cell cycle arrest and apoptosis. Furthermore, we found that Tic10 decreased the expression of CDK4 via FOXO3a-dependment mechanism. In addition, our data showed that Tic10 could sensitize drug resistant T47D/5-Fu cells to 5-Fu in vivo. Taken together, these data suggested Tic10 as capable of restoring sensitivity for drug-resistant breast cancer cells.

HSP27-Mediated Extracellular and Intracellular Signaling Pathways Synergistically Confer Chemoresistance in Squamous Cell Carcinoma of Tongue.

Purpose: Squamous cell carcinoma of tongue (SCCT) is the most common type of oral cavity carcinoma. Chemoresistance in SCCT is common, and the underlying mechanism remains largely unknown. We aimed to identify key molecules and signaling pathways mediating chemoresistance in SCCT.Experimental Design: Using a proteomic approach, we found that the HSP27 was a potential mediator for chemoresistance in SCCT cells. To further validate this role of HSP27, we performed various mechanistic studies using in vitro and in vivo models as well as serum and tissue samples from SCCT patients.Results: The HSP27 protein level was significantly increased in the multidrug-resistant SCCT cells and cell culture medium. Both HSP27 knockdown and anti-HSP27 antibody treatment reversed chemoresistance. Inversely, both HSP27 overexpression and recombinant human HSP27 protein treatment enhanced chemoresistance. Moreover, chemotherapy significantly induced HSP27 protein expression in both SCCT cells and their culture medium, as well as in tumor tissues and serum of SCCT patients. HSP27 overexpression predicts a poor outcome for SCCT patients receiving chemotherapy. Mechanically, extracellular HSP27 binds to TLR5 and then activates NF-κB signaling to maintain SCCT cell survival. TLR5 knockdown or restored IκBα protein level disrupts extracellular HSP27-induced NF-κB transactivation and chemoresistance. Moreover, intracellular HSP27 binds to BAX and BIM to repress their translocation to mitochondrion and subsequent cytochrome C release upon chemotherapy, resulting in inhibition of the mitochondrial apoptotic pathway.Conclusions: HSP27 plays a pivotal role in chemoresistance of SCCT cells via a synergistic extracellular and intracellular signaling. HSP27 may represent a potential biomarker and therapeutic target for precision SCCT treatment. Clin Cancer Res; 24(5); 1163-75. ©2017 AACR.

Epigenetic silencing of miR-493 increases the resistance to cisplatin in lung cancer by targeting tongue cancer resistance-related protein 1(TCRP1).

BACKGROUND: The potential mechanisms regarding how methylation of microRNA(miRNA) CpG Island could regulate cancer cell chemo-resistance remains unclear. This study aims to explore the epigenetic dysregulation mechanism of miRNA-493 and the ability to modulate lung cancer cell chemotherapy resistance. METHODS: Real-time quantitative PCR (qRT-PCR) and In situ hybridization (ISH) were used to analyze the expression of miR-493 in lung cancer cell lines and tumor tissue, respectively. Bisulfite sequencing PCR (BSP) was used to exam the promoter CpG Island of miR-493. The effect of miR-493 on chemosensitivity was evaluated by cell viability assays, apoptosis assays and in vivo experiment. The DNA damage was measured by γ-H2AX immunofluorescence. Luciferase reporter assay was used to assess the target genes of miR-493. Expression of target proteins and downstream molecules were analyzed by Western blot. RESULTS: miR-493 is silenced in resistant lung cancer cell due to the aberrant DNA methylation. Enforced expression of miR-493 in lung cancer cells promotes chemotherapy sensitivity to cisplatin through impairing the DNA damage repair and increasing the cells apoptosis in vitro and in vivo. Furthermore, we identify that TCRP1 is a direct functional target of miR-493. Ectopic expression of TCRP1 attenuated increased apoptosis in miR-493-overexpressing lung cancer cells upon cisplatin treatment. Meanwhile, miR-493 level is negatively correlated with TCRP1 expression in lung cancer patients and TCRP1 expression were correlated with poor survival. CONCLUSIONS: Our results highlight that hyper-methylation of miR-493CpG island might play important roles in the development of lung cancer chemo-resistance by targeting TCRP1, which might be used as a potential therapeutic target in preventing the chemo-resistance of lung cancer.

TCRP1 transcriptionally regulated by c-Myc confers cancer chemoresistance in tongue and lung cancer.

Previously, we cloned a new gene termed 'tongue cancer resistance-associated protein 1' (TCRP1), which modulates tumorigenesis, enhances cisplatin (cDDP) resistance in cancers, and may be a potential target for reversing drug resistance. However, the mechanisms for regulating TCRP1 expression remain unclear. Herein, we combined bioinformatics analysis with luciferase reporter assay and ChIP assay to determine that c-Myc could directly bind to TCRP1 promoter to upregulate its expression. TCRP1 upregulation in multidrug resistant tongue cancer cells (Tca8113/PYM) and cisplatin-resistant A549 lung cancer cells (A549/DDP) was accompanied by c-Myc upregulation, compared to respective parental cells. In tongue and lung cancer cells, siRNA-mediated knockdown of c-Myc led to decrease TCRP1 expression, whereas overexpression c-Myc did the opposite. Moreover, TCRP1 knockdown attenuated chemoresistance resulting from c-Myc overexpression, but TCRP1 overexpression impaired the effect of c-Myc knockdown on chemosensitivity. Additionally, in both human tongue and lung cancer tissues, c-Myc protein expression positively correlated with TCRP1 protein expression and these protein levels were associated with worse prognosis for patients. Combined, these findings suggest that c-Myc could transcriptionally regulate TCRP1 in cell lines and clinical samples and identified the c-Myc-TCRP1 axis as a negative biomarker of prognosis in tongue and lung cancers.

MYCN-mediated miR-21 overexpression enhances chemo-resistance via targeting CADM1 in tongue cancer.

Chemo-resistance is still a major obstacle in successful cancer treatment. Previously, we found that miR-21 (miR-21-5p) was upregulated in drug-resistant tongue cancer (TC) cell line Tca8113/PYM. However, the mechanisms for miR-21 upregulation and its role in chemo-resistance in TC remain unclear. Here, we demonstrated that functional inhibition of miR-21 sensitized TC cells to chemotherapy. In agreement, overexpressed miR-21 enhanced chemo-resistance in TC cells. We found that miR-21 directly targeted CADM1 expression, which was downregulated in drug-resistant TC cells. Restored CADM1 expression sensitized TC cells to chemotherapy, but CADM1 knockdown induced chemo-resistance. Mechanically, CADM1 interacted with BMI1 to inhibit its nuclear translocation. Moreover, MYCN which was overexpressed in drug-resistant TC cells directly bound to the miR-21 promoter to upregulated miR-21 expression in TC cells. Importantly, the expression levels of miR-21 and CADM1 negatively correlated, but MYCN and miR-21 positively correlated in TC tissues. High levels of miR-21 and MYCN and low level of CADM1 were associated with poor prognosis in TC patients. In conclusion, our study suggests an important role of the MYCN/miR-21/CADM1 axis in chemo-resistance in TC patients and may lead to promising prognostic biomarkers and novel treatment strategies to improve the chemotherapeutic efficacy for TC patients. KEY MESSAGES: MiR-21 enhances chemo-resistance via targeting CADM1 in tongue cancer cells. CADM1 sensitizes tongue cancer cells to chemotherapy. CADM1 interacts with BMI1 to inhibit its nuclear translocation. MYCN transcriptionally regulates miR-21 expression. Dysregulated MYCN/miR-21/CADM1 axis associates with poor prognosis in TC patients.

miR-493 mediated DKK1 down-regulation confers proliferation, invasion and chemo-resistance in gastric cancer cells.

In the present study, we demonstrated that the levels of DKK1 were decreased in serums and tissues of GC. DKK1 levels inversely correlated with tumor class, TNM stage, distant metastasis and lymph node metastasis of GC. GC patients with low DKK1 levels had a poor overall survival. DKK1 inhibited the proliferation of GC cells in vitro and in vivo. DKK1 also inhibited invasion, but enhanced chemo-sensitivity of GC cells. Mechanically, miR-493 levels increased in GC and directly targeted and down-regulated DKK1 expression. In agreement, miR-493 promoted proliferation of GC cells in vitro and in vivo. MiR-493 also promoted invasion and chemo-resistance of GC cells. However, DKK1 overexpression reversed the effects of miR-493 on proliferation, invasion and chemo-sensitivity. Thus, our results provide new insight for the role of miR-493/DKK1 axis in GC.

ZEB1 transcriptionally regulated carbonic anhydrase 9 mediates the chemoresistance of tongue cancer via maintaining intracellular pH.

BACKGROUND: Chemoresistance is a major obstacle in successfully treating cancers, and the mechanisms responsible for drug resistance are still far from understood. Carbonic anhydrase 9 (CA9) has been shown to be upregulated in the drug-resistant tongue cancer cell line Tca8113/PYM and to be associated with drug resistance. However, the mechanisms regulating CA9 expression and its role in drug resistance remain unclear. METHODS: Bioinformatic and experimental analysis involving ChIP and luciferase reporter assays were used to validate Zinc finger E-box-binding homeobox 1 (ZEB1) as a transcriptional regulator of CA9. Gene expression and protein levels were evaluated by quantitative RT-PCR and western blotting, respectively. Sensitivity to chemotherapy was examined using the MTS assay and Hoechst staining and analysis caspase-3 activity to evaluate changes in apoptosis. Intracellular pH (pHi) was measured using fluorescent pH-indicator BCECF-AM. Protein expression in patient tissue samples was examined by immunohistochemistry and survival of tongue cancer patients from which these samples were derived was also analyzed. RESULTS: ZEB1 bound to the promoter of CA9 to positively regulate CA9 expression in tongue cancer cells. Knockdown of CA9 using short interfering RNA (siRNA) abolished the chemoresistance resulting from ZEB1 overexpression in Tca8113 and SCC-25 cells, and CA9 overexpression attenuated chemosensitivity induced by ZEB1 knockdown in Tca8113/PYM cells. CA9 knockdown also prevented maintenance of pHi mediated by overexpression of ZEB1 in Tca8113 and SCC-25 cells following chemotherapy, associated with increased apoptosis and caspase-3 activation. Conversely, ectopic expression of CA9 suppressed decrease in pHi mediated by ZEB1 knockdown in Tca8113/PYM cells following chemotherapy, accompanied by decreased apoptosis and caspase-3 activation. Importantly, a positive correlation was observed between ZEB1 and CA9 protein expression in tongue cancer tissues, and expression of these proteins associated with a poor prognosis for patients. CONCLUSION: Our finding that tumor cells regulate pHi in response to chemotherapy provides new insights into mechanisms of drug resistance during cancer treatment. Identification of the ZEB1-CA9 signaling axis as a biomarker of poor prognosis in tongue cancer will be valuable in future development of therapeutic strategies aimed at improving treatment efficacy, especially in terms of drug resistance associated with this disease.

The miR-491-3p/mTORC2/FOXO1 regulatory loop modulates chemo-sensitivity in human tongue cancer.

We found that levels of miR-491-3p were decreased in multidrug-resistant tongue cancer (TC) cells. Induction of miR-491-3p expression sensitized TC cells to chemotherapy. In agreement, functional inhibition of miR-491-3p enhanced resistance of TC cells to chemotherapy. We found that miR-491-3p directly targeted mTORC2 component Rictor and inhibited mTORC2 activity, which was increased in resistant TC cells with high p-Akt(Ser473), p-SGK1(Ser422) and p-FOXO1(Thr24) levels. Inhibition of mTORC2 activity via either Rictor knockdown or mTOR inhibitor in turn sensitized TC cells to chemotherapy. In agreement, overexpression of Rictor increased the mTORC2 activity and induced resistance of TC cells to chemotherapy. As a feedback loop, mTORC2 downregulated miR-491-3p expression by inactivating FOXO1, which otherwise would transcriptionally induce miR-491-3p expression. Levels of miR-491-3 and Rictor or mTORC2 activity negatively correlated in TC tissues. Finally, low levels of miR-491-3p and highly expressed Rictor were associated with poor prognosis in tongue cancer patients. These data provide a rationale for targeted intervention on miR-491-3p/mTORC2 axis to enhance the efficacy of chemotherapy against tongue cancer.

[Studies on IFN-gamma-mediated reversion of CIK killing sensitivity to edited human lung cancer A549 cells].

AIM: To explore IFN-gamma-mediated reversion of CIK killing sensitivity to immunoedited lung cancer A549 cells. METHODS: RT-PCR and MTT methods were used to detect the effect on MICA mRNA expression induced by IFN-gamma in the edited A549 cells and the change of CIK killing sensitivity to A549 cells, respectively. RESULTS: Low expression of cell surface MICA and low killing sensitivity of CIKs were observed in edited A549 cells. IFN-gamma could significantly increase MICA mRNA expression in the edited A549 cells and improve CIK cell cytotoxicity. CONCLUSION: IFN-gamma could reverse CIK killing sensitivity to the edited A549 cells by enhancing the MICA mRNA expression.

[Effect of Fuzheng Peiben therapy on dendritic cell in patients with breast cancer].

OBJECTIVE: To investigate the repairing mechanism of Fuzheng Peiben Therapy on cellular immunofunction in patients with breast cancer on cellar and molecular level. METHODS: The tumor tissue and axillary lymph node samples were evaluated with the flow cytometry for CD83, CD80, CD86 before and after neoadujvant therapy. RESULTS: The levels of CD83, CD80, CD86 were singificantly decreased in group A (treated with surgery only), B (treated with neoadujvant chemotherapy plus surgery) and C (treated with neoadujvant chemotherapy plus surgery with shenqi Fuzheng Injection) compared with that in normal team (P < 0.05 or 0.01); The levels of CD83, CD80, CD86 were significantly decreased in group A, B and C compared between before and after neoadujvant chemotherapy (P < 0.05 or 0.01); They were not significantly decreased between group A and group C (P > 0.05). CONCLUSION: The cellular immunity was inpaired considerably by neoadujvant chemotherapy. Neoadjuvant chemotherapy combined with Shenqi Fuzheng Injection can enhance the cellular immunity considerably.

Clinical study on treatment of mammary cancer by shenqi fuzheng injection in cooperation with chemotherapy.

OBJECTIVE: To study the effect of Shenqi Fuzheng Injection (SFI) on cellular immune in patients with mammary cancer (MC) after chemotherapy. METHODS: One hundred and ten patients with MC were randomly assigned to two groups. The 58 patients in the tested group were treated with SFI in cooperation with chemotherapy of CAF protocol (Cyclophosphamide, Doxorubicin and Fluorouracil), while the 52 patients in the control group were treated with chemotherapy of the same protocol alone. Changes of the patients' quality of life (QOF), adverse reaction that occurred, peripheral lymphocyte count and killing activity of single karyocyte before and after treatment between the two groups were compared. RESULTS: Patients' QOF elevating rate after treatment in the tested group and the control group was 34.5% and 13.5% respectively; The lowering of peripheral blood cell count of WBC, platelet and lymphocyte as well as that of the killing activity of single peripheral karyocyte on various kinds of MC cells were all milder and recovery sooner than those in the control group. CONCLUSION: SFI in combination with chemotherapy in treating MC could reduce the occurrence of adverse reaction to chemotherapy, improve clinical symptoms, elevate QOF and enhance immunity in patients with MC.