Constitutive expression of hyaluronan binding protein 1 (HABP1/p32/gC1qR) in normal fibroblast cells perturbs its growth characteristics and induces apoptosis

Meenakshi, J; Anupama, .; Goswami, Shyamal; Datta, Kasturi

doi:10.1016/s0006-291x(02)02788-2

Cited by 53 publications

(51 citation statements)

References 28 publications

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“…The present study has shown that overexpression of HABP1 in the human liver cell line HepG2 (HepR21) induces high endogenous glutathione levels and enhanced cellular proliferation over longer periods of cell growth, contrary to F111 cells, where HABP1 overexpression leads to ROS-mediated apoptosis (13,15). A marked increase in the total "HA pool" and HA cable formation was seen in HepR21 cells, as reflected by HAS2 up-regulation and down-regulation of HYAL2 and HYAL3.…”

Section: Discussionmentioning

confidence: 63%

“…During clone propagation frequent media change was not required, unlike reported for F111 (13). Two of the stable transfectants, named clones 6 and 21, showed the most appropriate expression for Myc-tagged HABP1.…”

Section: Overexpression Of Habp1 Does Not Lead To Growthmentioning

confidence: 96%

“…Constitutive expression of HABP1 in the parent fibroblast cell line has been shown to inhibit cell growth, formation of vacuoles, and induction of apoptosis at 60 h in the absence of media replacement (13). Transient expression of HABP1 and its N and C terminus truncated variants in COS-1 cells were found to induce autophagic vacuoles and disruption of the F-actin network indicating a stress condition (14).…”

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confidence: 99%

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Overexpression of Hyaluronan-binding Protein 1 (HABP1/p32/gC1qR) in HepG2 Cells Leads to Increased Hyaluronan Synthesis and Cell Proliferation by Up-regulation of Cyclin D1 in AKT-dependent Pathway

Kaul

Saha

Mallampati

et al. 2012

Journal of Biological Chemistry

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Background: Hyaluronan (HA) levels regulate cell behavior, tumor invasion, and migration through interactions with hyaladherins. Results: Elevated expression of hyaluronan-binding protein 1 (HABP1) leads to enhanced HA synthesis, HA cable formation, and activation of cell survival pathways in HepG2 cells. Conclusion: Constitutively elevated expression of HABP1 leads to enhanced tumorigenic potential by HA-mediated pathways. Significance: HABP1 modulates cell survival through enhanced HA synthesis.

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Section: Discussionmentioning

confidence: 63%

Section: Overexpression Of Habp1 Does Not Lead To Growthmentioning

confidence: 96%

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confidence: 99%

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Overexpression of Hyaluronan-binding Protein 1 (HABP1/p32/gC1qR) in HepG2 Cells Leads to Increased Hyaluronan Synthesis and Cell Proliferation by Up-regulation of Cyclin D1 in AKT-dependent Pathway

Kaul

Saha

Mallampati

et al. 2012

Journal of Biological Chemistry

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“…This has been considered to be the induction of premature senescence. Cisplatin has been known as an anti-neoplastic drug against tumor cells [6,7]. Cisplatin-induced DNA damage was also reported in human fibroblast cells [7,8].…”

Section: Introductionmentioning

confidence: 99%

“…Cisplatin has been known as an anti-neoplastic drug against tumor cells [6,7]. Cisplatin-induced DNA damage was also reported in human fibroblast cells [7,8]. However, it is not known if cisplatin will trigger a cascade of senescence responses in normal cells.…”

Section: Introductionmentioning

confidence: 99%

Cisplatin-induced premature senescence with concomitant reduction of gap junctions in human fibroblasts

2004

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To examine the role of gap junctions in cell senescence, the changes of gap junctions in cisplatin-induced premature senescence of primary cultured fibroblasts were studied and compared with the replicative senescent human fibroblasts. Dye transfer assay for gap junction function and immunofluorescent staining for connexin 43 protein distribution were done respectively. Furthermore, cytofluorimetry and DAPI fluorescence staining were performed for cell cycle and apoptosis analysis. p53 gene expression level was detected with indirect immunofluorescence. We found that cisplatin (10 mM) treatment could block cell growth cycle at G1 and induced premature senescence. The premature senescence changes included high frequency of apoptosis, elevation of p53 expression, loss of membranous gap junctions and reduction of dye-transfer capacity. These changes were comparable to the changes of replicative senescence of human fibroblasts. It was also concluded that cisplatin could induce premature senescence concomitant with inhibition of gap junctions in the fibroblasts. Loss of functional gap junctions from the cell membrane may account for the reduced intercellular communication in the premature senescent fibroblasts. The cell system we used may provide a model useful for the study of the gap junction thus promoting agents against premature senescence.

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Low‐dose rotenone exposure induces early senescence leading to late apoptotic signaling cascade in human trabecular meshwork (HTM) cell line: An in vitro glaucoma model

Maurya

Agarwal

Ghosh

2015

Cell Biology International

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This study aimed to determine whether the prolonged exposure of the human trabecular meshwork (HTM) cell line to a low dose (1 nM) of rotenone could simulate a glaucomatous-like condition and serve as a cellular model for its etiological analysis. Under 1-nM rotenone exposure for 24-72 h, HTM cells showed a decrease in cell viability as assessed by an MTT assay and showed mitochondrial dysfunction as assessed by measuring H2 DCFDA fluorescence; a decrease in ATP level was also observed. Flow cytometric analysis showed an increase in cellular size and granularity. Elevated AF showed initial senescence. LF staining with SBB and its spectrofluorometric quantification confirmed growth arrest. An accumulation of cytoplasmic myocilin, IL-6, and MMP-9 at 72 h of exposure supported glaucomatous induction. TEM revealed morphological changes in mitochondria and nuclei of treated cells. Signaling cascades were assessed by immunoblotting and immunocytochemical analysis. This study showed a shift in status of the cells from initial senescence to induction of apoptosis in the HTM cell line due to continuous low-dose exposure to rotenone; however, at 72 h, both senescence and apoptotic features are apparent in these cells. This is the first report that reveals the potential of a prolonged low-dose exposure of rotenone to simulate senescence in the HTM cell line to cause a glaucomatous condition.

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Constitutive expression of hyaluronan binding protein 1 (HABP1/p32/gC1qR) in normal fibroblast cells perturbs its growth characteristics and induces apoptosis

Cited by 53 publications

References 28 publications

Overexpression of Hyaluronan-binding Protein 1 (HABP1/p32/gC1qR) in HepG2 Cells Leads to Increased Hyaluronan Synthesis and Cell Proliferation by Up-regulation of Cyclin D1 in AKT-dependent Pathway

Overexpression of Hyaluronan-binding Protein 1 (HABP1/p32/gC1qR) in HepG2 Cells Leads to Increased Hyaluronan Synthesis and Cell Proliferation by Up-regulation of Cyclin D1 in AKT-dependent Pathway

Cisplatin-induced premature senescence with concomitant reduction of gap junctions in human fibroblasts

Low‐dose rotenone exposure induces early senescence leading to late apoptotic signaling cascade in human trabecular meshwork (HTM) cell line: An in vitro glaucoma model

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