Preliminary studies on LED-activated pyropheophorbide-α methyl ester killing cisplatin-resistant ovarian carcinoma cells

In the present study, a novel LED source was applied for activating pyropheophorbids-a methyl ester (MPPa) in cisplatin-resistant ovarian cell line COC1/DDP cells. MPPa concentration was 2 μM and light energy from 0.125–8 J/cm². Cytotoxicity was investigated 24 h using MTT reduction assay and light microscopy after treatment. Cellular ultrastructure was observed using transmission electron microscopy (TEM) and nuclear chromatin by fluorescent microscope with Hoechst33258 staining. MTT reduction assay showed that the cytotoxicity of LED-activated MPPa in the COC1/DDP cells increased along with the light dose of LED source and LED-activated MPPa resulted in light-dependent cytotoxicity. The observations from light microscopy reinforced the above results. TEM showed that necrotic cells with the disruption of karyotheca, karyorrhexis, and karyolysis of nucleus and apoptotic cells, especially the apoptotic body, can be seen post LED-activated MPPa. Hoechst33258 staining showed that condensation of chromatin and nuclear fragmentations could be found in many treated cells and some of them formed the structure of apoptotic bodies when COC1/DDP cells were exposed to 2 μM MPPa for 20 h and then 1 J/cm² irradiation of LED source. The findings demonstrated that the novel LED source could efficiently activated MPPa and LED-activated MPPa could significantly kill cisplatin-resistant ovarian cell line COC1/DDP cells through two major pathways including necrosis and apoptosis, suggesting that LED is a novel and efficient light source and LED-activated MPPa might be potential therapeutic modality for treating cisplatin-resistant ovarian carcinoma.     

Apoptosis of ovarian cancer cells induced by methylene blue-mediated sonodynamic action

Objective

The present study aims to investigate apoptosis of ovarian cancer cells induced by methylene blue (MB)-mediated sonodynamic therapy (SDT).

Methods

The MB concentration was kept constant at 100 μM and ovarian cancer HO-8910 cells were exposed to ultrasound therapy for 5 s with an intensity of 0.46 W/cm². The cytotoxicity was investigated 24 h after MB-mediated sonodynamic action. Apoptosis was analyzed using a flow cytometer with Annexin V-FITC and propidium iodine (PI) staining as well as fluorescence microscopy with Hoechst 33258 staining. Intracellular reactive oxygen species (ROS) level was measured by flow cytometer with 2,7-dichlorodihydrofluorescein diacetate (DCFH-DA) staining.

Results

The cytotoxicity of MB-mediated SDT on HO-8910 cells after MB-mediated SDT was significantly higher than those of other treatments including ultrasound alone, MB alone and sham treatment. Flow cytometric analysis showed a significant increase in the early and late apoptotic cell populations by MB-mediated SDT of HO-8910 cells. Nuclear condensation and increased ROS levels were also found in HO-8910 cells treated by MB-mediated SDT.

Conclusions

Our findings demonstrated that MB-mediated sonodynamic action significantly induced apoptosis of HO-8910 cells and an increase in intracellular ROS level. This indicates that apoptosis is an important mechanism of cell death induced by MB-mediated SDT. Thus, MB-mediated SDT might be a potential therapeutic strategy for combating ovarian cancer.     

Effect of blue light radiation on curcumin-induced cell death of breast cancer cells

In the present study, we have successfully set up a novel blue light source with the power density of 9 mW/cm² and the wavelength of 435.8 nm and then the novel light source was used to investigate the effect of light radiation on curcumin-induced cell death. The cytotoxicity was investigated 24 h after the treatment of curcumin and blue light radiation together using MTT reduction assay. Nuclear chromatin was observed using a fluorescent microscopy with Hoechst33258 staining. The results showed blue light radiation could significantly enhance the cytotoxicity of curcumin on the MCF-7 cells and apoptosis induction. These findings demonstrated that blue light radiation could enhance curcumin-induced cell death of breast cancer cells, suggesting light radiation may be an efficient enhancer of curcumin in the management of breast cancer.     

Hypocrellin B-mediated sonodynamic action induces apoptosis of hepatocellular carcinoma cells

Objective

The present study aims to investigate apoptosis of hepatocellular carcinoma cells induced by hypocrellin B-mediated sonodynamic action.

Methods

The hypocrellin B concentration was kept constant at 2.5 μM and cells from the hepatocellular carcinoma HepG2 cell line were exposed to ultrasound with an intensity of 0.46 W/cm² for 8 s. Cell cytotoxicity was quantified using an MTT assay 24 h after sonodynamic therapy (SDT) of hypocrellin B. Apoptosis was investigated using a flow cytometry with Annexin V-FITC and propidium iodine staining. Intracellular reactive oxygen species (ROS) levels were detected using a flow cytometry with 2,7-dichlorodihydrofluorecein diacetate (DCFH-DA) staining.

Results

The cytotoxicity of hypocrellin B-mediated sonodynamic action on HepG2 cells was significantly higher than those of other treatments including ultrasound alone, hypocrellin B alone and sham treatment. Flow cytometry showed that hypocrellin B-induced sonodynamic action markedly enhanced the apoptotic rate of HepG2 cells. Increased ROS was observed in HepG2 cells after being treated with hypocrellin B-mediated sonodynamic action.

Conclusions

Our data demonstrated that hypocrellin B-mediated sonodynamic action remarkably induced apoptosis of HepG2 cells, suggesting that apoptosis is an important mechanism of cell death induced by hypocrellin B-mediated SDT.     

Blue light-activated hypocrellin B damages ovarian cancer cells

In the present study, a novel blue light source from LED was used to activate hypocrellin B in ovarian cancer HO-8910 cells. Hypporellin B concentration was kept at 2.5 μM and light doses from 0.5–4.0 J/cm². Photocytotoxicity was investigated using MTT reduction assay and light microscopy after light irradiation. Cellular morphology was observed using transmission electron microscopy (TEM). MTT assay showed that the cytotoxicity of blue light-activated hypocrellin B in HO-8910 cells increased along with light dose. The observations from light microscopy reinforced the above results. TEM showed that microvillin disappearance, vacuole formation, chromatin condensation, and topical apoptotic body were observed in the cells treated by both light and hypocrellin B. The findings demonstrated that blue light from LED source could effectively activate hypocrellin B to cause the destruction of HO-8910 cells, indicating that Blue light-activated hypocrellin B might be potential therapeutic strategy in the management of ovarian cancer.     

Sonodynamic action of pyropheophorbide-a methyl ester induces mitochondrial damage in liver cancer cells

Sonodynamic therapy with pyropheophorbide-a methyl ester (MPPa) presents a promising aspect in treating liver cancer. The present study aims to investigate the mitochondrial damage of liver cancer cells induced by MPPa-mediated sonodynamic action. Mouse hepatoma cell line H₂₂ cells were incubated with MPPa (2 μM) for 20 h and then exposed to ultrasound with an intensity of 0.97 W/cm² for 8 s. Cytotoxicity was investigated 24 h after sonodynamic action using MTT assay and light microscopy. Mitochondrial membrane potential (ΔΨm) was analyzed using flow cytometry with rhodamine 123 staining and ultrastructural changes were observed using transmission electron microscopy (TEM).The cytotoxicity of MPPa-mediated SDT on H₂₂ cell line was 73.00 ± 3.42%, greater than ultrasound treatment alone (28.12 ± 5.19%) significantly while MPPa treatment alone had no significant effect on H₂₂ cells. Moreover, after MPPa-mediated SDT cancer cells showed swollen mitochondria under TEM and a significant collapse of mitochondrial membrane potential. Our findings demonstrated that MPPa-mediated SDT could remarkably induce cell death of H₂₂ cells, and highlighted that mitochondrial damage might be an important cause of cell death induced by MPPa-mediated SDT.     

The effects of Ce6-mediated sono-photodynamic therapy on cell migration,apoptosis and autophagy in mouse mammary 4T1 cell line

Purpose

Sono-Photodynamic therapy (SPDT) is an alternative therapy which claims to enhance the anti-cancer effects by combining sonodynamic therapy (SDT) with photodynamic therapy (PDT). In the present study, we investigated the effects of chlorin e6 (Ce6) mediated SPDT on migration, apoptosis and autophagy in mouse mammary 4T1 cancer cells, and its underlying mechanisms.

Materials

Cell migration was determined by wound healing assay. Apoptosis was analyzed using annexin V-PE/7-ADD staining as well as Hoechst 33342 staining. Changes of mitochondria membrane potential (MMP) was evaluated by flow cytometry. Formation of acidic vesicular organelles (AVOs) during autophagy was observed with fluorescence microscope by MDC staining. Immunofluorescence assays were performed to detect the co-localization of LC3 and Lamp2. Western blotting was employed to analyze the activity of the apoptosis related proteins Caspase-3, PARP, Bax and Bcl-2, as well as the autophagy associated processing of LC3-I to LC3-II and Beclin-1 expression.

Results

Ce6 mediated SPDT further enhanced cell migration inhibition, significantly triggered cell apoptosis, nuclear condensation and MMP drop. Cleaved Caspase-3 and PARP increased dramatically after Ce6-SPDT, accompanied by decreased Bcl-2 expression, while the expression of Bax remained stable. Additionally, AVOs formation, co-localization of LC3 and Lamp2 occurred following Ce6-SPDT and simultaneously accompanied by LC3-II processing and increased Beclin-1 expression.

Conclusions

Ce6-SPDT could enhance cell migration inhibition, and induce mitochondria-dependent apoptosis as well as autophagy in 4T1 cells.     

Protoporphyrin IX-mediated sonodynamic action induces apoptosis of K562 cells

Objectives

The present study aims to investigate apoptosis of human leukemia K562 cells induced by protoporphyrin IX (PpIX)-mediated sonodynamic therapy (PpIX-SDT).

Methods

The uptakes of intracellular PpIX in K562 cells were detected by flow cytometry. The sub-cellular localization of PpIX was imaged by confocal microscope. The cytotoxic effect of PpIX-SDT was assessed by MTT (3-(4,5-dimethylthiazol-2-yl)-2, 5-diphenylter-trazolium bromide tetrazolium) assay. Apoptosis was evaluated by chromatin condensation with DAPI (4′-6-diamidino-2-phenylindole) staining, decrease of mitochondria membrane potential (MMP), re-distribution of Bax, and the expression changes of the key apoptosis-associated protein (Caspase-3 and polypeptide poly (ADP-robose) polymerase). The possible mechanism of SDT-induced apoptosis was investigated by detecting by intracellular ROS (reactive oxygen species) generation and effect of ROS scavenger-NAC (N-acetylcysteine) on SDT induced apoptosis.

Results

The intracellular PpIX increased quickly within 2 h after PpIX administration and PpIX mainly localized in the mitochondria. Compared with PpIX alone and ultrasound alone groups, the synergistic cytotoxicity of PpIX plus ultrasound was significantly boosted. In addition, the ultrasound induced some extent of chromatin condensation and MMP loss was greatly enhanced by the presence of 2 μg/ml PpIX, where PpIX alone treatment showed no or only slight effect. Time-dependent Bax translocation, caspase-3 activation and PARP cleavage were detected in SDT treatment groups. Besides, intracellular ROS production was significantly enhanced after SDT, and the general ROS scavenger NAC could obviously alleviate the SDT-caused cell viability loss, MMP loss, Bax redistribution and nuclear changes.

Conclusions

These results indicated that PpIX-mediated sonodynamic action could induce apoptosis on K562 cells, and the intracellular ROS was involved in the PpIX-SDT induced apoptosis.     

Targeted microbubbles for ultrasound mediated gene transfection and apoptosis induction in ovarian cancer cells

Ultrasound-targeted microbubble destruction (UTMD) technique can be potentially used for non-viral delivery of gene therapy. Targeting wild-type p53 (wtp53) tumor suppressor gene may provide a clinically promising treatment for patients with ovarian cancer. However, UTMD mediated gene therapy typically uses non-targeted microbubbles with suboptimal gene transfection efficiency. We synthesized a targeted microbubble agent for UTMD mediated wtp53 gene therapy in ovarian cancer cells. Lipid microbubbles were conjugated with a Luteinizing Hormone–Releasing Hormone analog (LHRHa) via an avidin–biotin linkage to target the ovarian cancer A2780/DDP cells that express LHRH receptors. The microbubbles were mixed with the pEGFP-N1-wtp53 plasmid. Upon exposure to 1 MHz pulsed ultrasound beam (0.5 W/cm²) for 30 s, the wtp53 gene was transfected to the ovarian cancer cells. The transfection efficiency was (43.90 ± 6.19)%. The expression of wtp53 mRNA after transfection was (97.08 ± 12.18)%. The cell apoptosis rate after gene therapy was (39.67 ± 5.95)%. In comparison with the other treatment groups, ultrasound mediation of targeted microbubbles yielded higher transfection efficiency and higher cell apoptosis rate (p < 0.05). Our experiment verifies the hypothesis that ultrasound mediation of targeted microbubbles will enhance the gene transfection efficiency in ovarian cancer cells.     

Effects of hydroxyapatite nanoparticles on proliferation and apoptosis of human breast cancer cells (MCF-7)

The study aimed to correlate cell proliferation inhibition with oxidative stress and p53 protein expression in cancerous cells. Hydroxyapatite (HAP) (Ca₁₀(PO₄)₆(OH)₂) is the essential component of inorganic composition in human bone. It has been found to have obvious inhibitory function on growth of many kinds of tumor cells and its nanoparticle has stronger anti-cancerous effect than macromolecule microparticles. Human breast cancer cells (MCF-7) were cultured and treated with HAP nanoparticles at various concentrations. Cells viability was detected with MTT colorimetric assay. The morphology of the cancerous cells was performed by transmission electron microscopy and the expression of a cell apoptosis related gene (p53) was determined by ELISA assay and flow cytometry (FCM). The intracellular reactive oxygen species (ROS) level in HAP exposed cells was measured by H₂DCFDA staining. DNA damage was measured by single-cell gel electrophoresis assay. The statistical analysis was done by one way ANOVA. The cellular proliferation inhibition rate was significantly (p < 0.05) increasing in a dose-dependent manner of HAP nanoparticles. Cell apoptotic characters were observed after MCF-7 cells were treated by HAP nanoparticles for 48 h. Moreover, ELISA assay and FCM shows a dose-dependent activation of p53 in MCF-7 cells treated with nanoHAP. These causative factors of the above results may be justified by an overproduction of ROS. In this study, a significant (p < 0.05) increase in the level of intracellular ROS in HAP-treated cells was observed. This study shows that HAP inhibits the growth of human breast cancer MCF-7 cells as well as induces cell apoptosis. This study shows that HAP NPs Induce the production of intracellular reactive oxygen species and activate p53, which may be responsible for DNA damage and cell apoptosis.     

Oxygen and Indocyanine Green loaded microparticles for dual-mode imaging and sonodynamic treatment of cancer cells

Oxygen and Indocyanine Green (ICG) loaded microparticles (OI-MPs) were fabricated by a gas-driven coaxial flow focusing (CFF) process for dual-mode imaging and sonodynamic therapy (SDT). The produced OI-MPs agent showed stable optical properties, superior imaging depth in near infrared (NIR) fluorescence imaging, and enhanced acoustic contrast after ultrasound mediation. We hypothesized that encapsulating ICG and oxygen in microparticles would enhance reactive oxygen species (ROS) production in SDT. This hypothesis was validated in a cell-free environment. We further hypothesized that ultrasound mediated fragmentation of the OI-MPs would induce cytotoxicity and apoptosis of cancer cells. This hypothesis was validated in SKOV3 ovarian cancer cells. Our research demonstrated that OI-MPs can be potentially used as a dual-mode theranostic agent for image guided SDT with enhanced efficacy. Further study is needed to delineate the mechanism of ROS-induced cell apoptosis and optimize the OI-MPs formulation for the maximal anti-cancer potency.     

5-Aminolaevulinic acid enhances ultrasound-induced mitochondrial damage in K562 cells

Background

Ultrasound therapy is a new modality in the control of malignant cancers. The aim of the present study was to investigate the effect of 5-aminolaevulinic acid on the ultrasonic killing action in the cancer cells.

Materials/methods

The K562 cells as a cancer cell model were subjected to investigate the effect of 5-aminolaevulinic acid (5-ALA) on the ultrasonic killing action, in which the 5-ALA concentration was 2 mM and the ultrasound exposure was 15 s at the intensity of 0.46 W/cm² and the frequency of 1.7 MHz. Cytotoxicity was investigated 24 h after ultrasound exposure using the trypan blue exclusion test. Ultrastructural cell morphology and mitochondrial changes were observed using transmission electron microscopy (TEM). Mitochondrial membrane potential (ΔΨm) was evaluated using Rhodamine 123 assay.

Results

The death rates of the K562 cells in the controls including sham radiation and 5-ALA treatment alone were 1.81 ± 0.13%, 1.27 ± 0.20%, respectively. Those in ultrasound radiation alone and 5-ALA-ultrasound treatment were 12.61 ± 2.63%, 46.87 ± 4.09%, respectively. There were significant differences between 5-ALA-ultrasound treatment, ultrasound radiation alone and the controls (P < 0.05). TEM showed that the mitochondria expanding and some vacuoles were found in the ultrasound-treated cells. After the treatment of ultrasound and 5-ALA together some cells presented typical characteristics of apoptotic cells, such as nuclear condensation and crescent formation. Mitochondria of the cells were damaged more seriously than those treated by ultrasound alone, there were obvious swollen mitochondria and mitochondria in which cristae were almost perfectly disappeared, and more vacuolar mitochondria were founded. Mitochondrial membrane potential (ΔΨm) was more significantly collapsed when the K562 cells were exposed to 2 mM 5-ALA for 4 h and then 0.46 W/cm² irradiation of ultrasound than ultrasound radiation alone.

Conclusion

5-ALA pretreatment significantly enhanced the cytotoxicity of ultrasound radiation in K562 cells. The damage of mitochondria structure and function might be an important cause of cell death in K562 cells induced by the treatment of ultrasound radiation and 5-ALA together.     

利用拉曼光谱分析顺铂诱导的胃癌细胞凋亡

利用激光拉曼光谱对顺铂诱导的胃癌细胞凋亡进行分析,胃癌细胞SGC7901经10 μg·mL-1顺铂处理24, 48, 72 h后,一部分用于荧光染色,另一部分用扫描方式收集细胞的拉曼光谱。光谱结果依次经背景扣除、平滑、归一化、基线校正、峰拟合等方法预处理。荧光染色结果显示对照组细胞核染色均匀,而药物处理72 h后,核碎裂,呈致密浓染。拉曼光谱结果显示顺铂处理24, 48, 72 h后,与核酸及蛋白质相关的峰均有降低,其中783, 1 002, 1 343 cm-1峰72 h后依次降低为初始值的52%,64%,76%,表明顺铂能够诱导胃癌细胞凋亡,凋亡细胞内核酸和蛋白质含量降低。以上结果说明,拉曼光谱能提供生物细胞内物质变化的丰富信息,是实时检测细胞凋亡过程的有效手段。     

Cytotoxicity and Cellular Uptake of Amorphous Silica Nanoparticles in Human Cancer Cells

The cytotoxic effects of silica nanoparticles (SNPs) on different human cancer cells, as well as the uptake kinetics and pathways of SNPs have been studied here. SNPs with the diameter of ≈20 nm induced a dose‐dependent cytotoxicity in both gastric cancer cells (MGC80–3) and cervical adenocarcinoma epithelial cells (HeLa), but MGC80–3 cells were more susceptible to the cytotoxic effect induced by SNPs. Changes in the nuclear morphology and flow cytometric analysis with annexin V/PI double staining show that SNPs induced a higher degree of apoptosis in MGC80–3 cells. Accordingly, more remarkable reactive oxygen species (ROS) burst is detected in SNP‐treated MGC80–3 cells. Using fluorescein isothiocyanate (FITC)‐labeled SNPs and flow cytometry, it is found that the uptake of SNPs is more efficient in MGC80–3 than in HeLa cells. SNPs are internalized into both cancer cells through energy‐dependent pathway. Inhibitor studies with dynasore and methyl‐β‐cyclodextrin show that these cancer cells took up 20 nm SNPs mainly through the caveolin‐mediated endocytosis, while in HeLa cells SNPs internalization was also via dynamin‐dependent clathrin‐mediated pathway. These findings indicate that SNPs cause differential cytotoxic effects in different human cancer cells, which might be related to the uptake process and efficiency toward these cancer cells.     

Deposition pressure effect on the surface roughness scaling of microcrystalline silicon films

The scaling behaviour of surface roughness evolution of microcrystalline silicon (μc-Si:H) films prepared by very-high frequency plasma-enhanced chemical vapour deposition (VHF-PECVD) has been investigated by using a spectroscopic ellipsometry (SE) technique. The growth exponent β was analysed for the films deposited under different pressures P_g. The results suggest that films deposited at P_g = 70 Pa have a growth exponent β about 0.22, which corresponds to the definite diffusion growth. However, abnormal scaling behaviour occurs in the films deposited at P_g = 300 Pa. The exponent β is about 0.81 that is much larger than 0.5 of zero diffusion limit in the scaling theory. The growth mode of μ c-Si:H deposited at P_g= 300 Pa is clearly different from that of μc-Si:H at P_g = 70 Pa. Monte Carlo simulations indicate that the sticking process and the surface diffusion of the radicals are two key factors to affect the growth mode under different pressures. Under P_g= 300 Pa, β>0.5 is correlated with the strong shadowing effect resulting from the larger sticking coefficient.     

Photodynamic action of LED-activated nanoscale photosensitizer in nasopharyngeal carcinoma cells

Background  

Photodynamic therapy has been confirmed to an efficient therapeutic modality of malignant tumors. The aim of the present study was to explore the photodynamic action of LED-activated nanoscale photosensitizer-loading hypocrellin in nasopharyngeal carcinoma cells.     

Particle Size of X-ray Pumped UVC-Emitting Nanoparticles Defines Intracellular Localization and Biological Activity Against Cancer Cells

Effectiveness of radiation treatment for cancer is limited in hypoxic tumors. Previous data shows that UVC-emitting nanoparticles enhance cytotoxicity of X-ray irradiation in hypoxic tumor cells. This study examines the impact on cell killing, particle size, uptake into cells, incubation time, and UV emission intensity of LuPO₄:Pr³⁺,Nd³⁺. A549 cells are treated with LuPO₄:Pr³⁺,Nd³⁺ and X-rays. The surviving fraction is evaluated using the colony formation assay after treatment of cells with different particle sizes (D₅₀ = 0.16 and 5.05 µm) and after different incubation times before X-ray irradiation. Nanoparticle uptake into cells is verified by transmission electron microscopy and quantified by inductively coupled plasma mass spectrometry. The microparticles exhibit a five times higher emission intensity compared to nanoparticles. Both particle sizes show an increased cytotoxic effect after X-ray excitation with prolonged incubation times. Surprisingly, the smaller nanoparticles show a significantly higher biological effect compared to the larger particles, despite their significantly lower UVC emission. Nanoparticles accumulate more quickly and closer to the nucleus than the microparticles, resulting in higher localized UVC emission and greater lethality. The results suggest that the number of intracellular particles and their proximity to the cell DNA is more important than the emission intensity of the particles.     

In vitro studies of Photofrin® mediated photodynamic therapy on human rhabdomyosarcoma cell line (RD)

In the current study, the cytotoxic effects induced by the given photosensitizer (PS) on human rhybdomyosarcoma cancer cells (RD) as an experimental model were investigated. The experimental results like cytotoxic effects induced by the given PS on RD cells were dose dependent and the optimum concentration of Photofrin® (100 μg/ml) along with 120 J/cm² generates the maximum loss in cell viability which is almost 82%. The significant loss in cell viability is the result of interaction of suitable dose of laser light (630 nm of wavelength) with Photofrin®, after excitation of PS, production of reactive oxygen species (ROS), which leads to mitochondria damage and resulting of cell death (cell necrosis/cell apoptosis). Viability of controlled and treated RD cells with optimum dose of light (630 nm) has been assessed by neutral red assay (NRA) and cell damaging effect were verified by staining of mitochondria using Mitotracker® red as an efficient dye as well as reactive oxygen species (ROS) accumulation detection.     

Substrate-dependent cell elasticity measured by optical tweezers indentation

In the last decade, cell elasticity has been widely investigated as a potential label free indicator for cellular alteration in different diseases, cancer included. Cell elasticity can be locally measured by pulling membrane tethers, stretching or indenting the cell using optical tweezers. In this paper, we propose a simple approach to perform cell indentation at pN forces by axially moving the cell against a trapped microbead. The elastic modulus is calculated using the Hertz-model. Besides the axial component, the setup also allows us to examine the lateral cell–bead interaction. This technique has been applied to measure the local elasticity of HBL-100 cells, an immortalized human cell line, originally derived from the milk of a woman with no evidence of breast cancer lesions. In addition, we have studied the influence of substrate stiffness on cell elasticity by performing experiments on cells cultured on two substrates, bare and collagen-coated, having different stiffness. The mean value of the cell elastic modulus measured during indentation was 26±9 Pa for the bare substrate, while for the collagen-coated substrate it diminished to 19±7 Pa. The same trend was obtained for the elastic modulus measured during the retraction of the cell: 23±10 Pa and 13±7 Pa, respectively. These results show the cells adapt their stiffness to that of the substrate and demonstrate the potential of this setup for low-force probing of modifications to cell mechanics induced by the surrounding environment (e.g. extracellular matrix or other cells).