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| 2. |
- Klionsky, Daniel J., et al.
(författare)
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Guidelines for the use and interpretation of assays for monitoring autophagy
- 2012
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Ingår i: Autophagy. - : Informa UK Limited. - 1554-8635 .- 1554-8627. ; 8:4, s. 445-544
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Forskningsöversikt (refereegranskat)abstract
- In 2008 we published the first set of guidelines for standardizing research in autophagy. Since then, research on this topic has continued to accelerate, and many new scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Accordingly, it is important to update these guidelines for monitoring autophagy in different organisms. Various reviews have described the range of assays that have been used for this purpose. Nevertheless, there continues to be confusion regarding acceptable methods to measure autophagy, especially in multicellular eukaryotes. A key point that needs to be emphasized is that there is a difference between measurements that monitor the numbers or volume of autophagic elements (e.g., autophagosomes or autolysosomes) at any stage of the autophagic process vs. those that measure flux through the autophagy pathway (i.e., the complete process); thus, a block in macroautophagy that results in autophagosome accumulation needs to be differentiated from stimuli that result in increased autophagic activity, defined as increased autophagy induction coupled with increased delivery to, and degradation within, lysosomes (in most higher eukaryotes and some protists such as Dictyostelium) or the vacuole (in plants and fungi). In other words, it is especially important that investigators new to the field understand that the appearance of more autophagosomes does not necessarily equate with more autophagy. In fact, in many cases, autophagosomes accumulate because of a block in trafficking to lysosomes without a concomitant change in autophagosome biogenesis, whereas an increase in autolysosomes may reflect a reduction in degradative activity. Here, we present a set of guidelines for the selection and interpretation of methods for use by investigators who aim to examine macroautophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes. These guidelines are not meant to be a formulaic set of rules, because the appropriate assays depend in part on the question being asked and the system being used. In addition, we emphasize that no individual assay is guaranteed to be the most appropriate one in every situation, and we strongly recommend the use of multiple assays to monitor autophagy. In these guidelines, we consider these various methods of assessing autophagy and what information can, or cannot, be obtained from them. Finally, by discussing the merits and limits of particular autophagy assays, we hope to encourage technical innovation in the field.
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| 3. |
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- 2019
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Tidskriftsartikel (refereegranskat)
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| 4. |
- Ding, Zhen-Yu, et al.
(författare)
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Livin expression is an independent factor in rectal cancer patients with or without preoperative radiotherapy
- 2013
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Ingår i: Radiation Oncology. - London, United Kingdom : BioMed Central. - 1748-717X. ; 8:1
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Tidskriftsartikel (refereegranskat)abstract
- Background: This study was aimed to investigate the expression significance of Livin in relation to radiotherapy (RT), clinicopathological and biological factors of rectal cancer patients.Methods: This study included 144 primary rectal cancer patients who participated in a Swedish clinical trial of preoperative radiotherapy. Tissue microarray samples from the excised primary rectal cancers, normal mucosa and lymph node metastases were immunostained with Livin antibody. The proliferation of colon cancer cell lines SW620 and RKO was assayed after Livin knock-down.Results: The expression of Livin was significantly increased from adjacent (P = 0.051) or distant (P = 0.028) normal mucosa to primary tumors. 15.4% (2/13) and 39.7% (52/131) patients with Livin-negative and positive tumors died at 180 months after surgery, and the difference tended to be statistically significant (P = 0.091). In multivariate analyses, the difference achieved statistical significance, independent of TNM stage, local and distant recurrence, grade of differentiation, gender, and age (odds ratio = 5.09, 95% CI: 1.01-25.64, P = 0.048). The in vitro study indicated colon cancer cells with Livin knock-down exhibited decreased proliferation compared with controls after RT.Conclusions: The expression of Livin was was independently related to survival in rectal cancer patients, suggesting Livin as a useful prognostic factor for rectal cancer patients.
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| 5. |
- Ding, Zhen-Yu, et al.
(författare)
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Upregulation of the antiapoptotic factor Livin contributes to cisplatin resistance in colon cancer cells
- 2013
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Ingår i: Tumor Biology. - : Karger / Springer Verlag (Germany). - 1010-4283 .- 1423-0380. ; 34:2, s. 683-693
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Tidskriftsartikel (refereegranskat)abstract
- The antiapoptotic factor Livin has been considered critical for tumor progression and poor prognosis for variant types of tumors. However, there are only limited reports regarding its expression and biological functions in colon cancer. Here, we examined Livin expression in four colon cancer cell lines (HCT116, RKO, KM12C, and SW620) in the presence or absence of cisplatin that was used as a model reagent. We found the different response to cisplatin was related to endogenous Livin expression level. From among a panel of apoptosis-related factors (p53, Bcl-2, Bcl-XL, BAX, and survivin), the expression of Livin was upregulated after cisplatin treatment in a dose-dependent manner. Both immunocytochemistry and nuclear cytoplasmic fractionation indicated Livin remained in the cytoplasm after treatment with cisplatin. In an attempt to explore the mechanism, we found the elevated expression of Livin was not due to the decreased degradation by proteosome but was enhanced at the mRNA level. Besides, cisplatin treatment activated the mammalian target of rapamycin (mTOR) pathway as shown by increased phosphorylation of Akt1, mTOR, S6K, and 4E-BP1, together with the elevated Livin. The PI3K inhibitor LY294002 inhibited both the phosphorylation of mTOR and upregulation of Livin. The stable overexpression of Livin inhibited the activation of caspase-3 and led to resistance to cisplatin, while the knockdown of Livin by siRNA rendered colon cancer cells more sensitive to cisplatin. Our study, along with others, highlighted the potential of Livin for cancer therapy in colon cancer.
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| 6. |
- Loof, Jasmine, et al.
(författare)
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Effects of Delta Np73 beta on cisplatin treatment in colon cancer cells
- 2012
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Ingår i: Molecular Carcinogenesis. - : Wiley-Blackwell. - 0899-1987 .- 1098-2744. ; 51:8, s. 628-635
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Tidskriftsartikel (refereegranskat)abstract
- p73 can activate transcription of p53-responsive genes, thereby inhibiting cell growth. An alternative promoter in the TP73 gene gives rise to an N-terminally truncated isoform of p73, Delta Np73, which lacks the transactivation domain of the full length TAp73 protein. TAp73 is considered pro-apoptotic, and Delta Np73 anti-apoptotic. In this study, we overexpressed ?Np73 beta in p53 wild type and p53 mutant colon cancer cell lines and further exposed the cells to cancer therapeutic drug cisplatin. The results showed that cisplatin decreased the protein expression levels of Delta Np73 beta in a dose-dependent manner, and both TAp73 and p53 were upregulated after cisplatin treatment. Further, clonogenic potential and cell viability were decreased, and apoptotic cells increased, in p53 mutant and in p53 wild type cells. Cellular viability was significantly higher in Delta Np73 beta-cells than mock-transfected cells. However, Delta Np73 beta overexpression did not affect the cellular susceptibility to cisplatin. In conclusion, the overexpression of Delta Np73 beta increases viability in p53 wild type and p53 mutant colon cancer cells, and cisplatin induces the degradation of Delta Np73 beta in a dose-dependent manner.
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| 7. |
- Meng, Wen-Jian, et al.
(författare)
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Special AT-rich sequence binding protein 1 expression correlates with response to preoperative radiotherapy and clinical outcome in rectal cancer
- 2015
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Ingår i: Cancer Biology & Therapy. - : Taylor & Francis. - 1538-4047 .- 1555-8576. ; 16:12, s. 1738-1745
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Tidskriftsartikel (refereegranskat)abstract
- Our recent study showed the important role of special AT-rich sequence binding protein 1 (SATB1) in the progression of human rectal cancer. However, the value of SATB1 in response to radiotherapy (RT) for rectal cancer hasn't been reported so far. Here, SATB1 was determined using immunohistochemistry in normal mucosa, biopsy, primary cancer, and lymph node metastasis from 132 rectal cancer patients: 66 with and 66 without preoperative RT before surgery. The effect of SATB1 knockdown on radiosensitivity was assessed by proliferation-based assay and clonogenic assay. The results showed that SATB1 increased from normal mucosa to primary cancer, whereas it decreased from primary cancer to metastasis in non-RT patients. SATB1 decreased in primary cancers after RT. In RT patients, positive SATB1 was independently associated with decreased response to preoperative RT, early time to metastasis, and worse survival. SATB1 negatively correlated with ataxia telangiectasia mutated (ATM) and pRb2/p130, and positively with Ki-67 and Survivin in RT patients, and their potential interaction through different canonical pathways was identified in network ideogram. Taken together, our findings disclose for the first time that radiation decreases SATB1 expression and sensitizes cancer cells to confer clinical benefit of patients, suggesting that SATB1 is predictive of response to preoperative RT and clinical outcome in rectal cancer.
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| 8. |
- Tseng, Chiao-Wei, et al.
(författare)
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Synergy of Ionic and Dipolar Effects by Molecular Design for pH Sensing beyond the Nernstian Limit
- 2020
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Ingår i: Advanced Science. - : Wiley. - 2198-3844. ; 7:2
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Tidskriftsartikel (refereegranskat)abstract
- Knowledge of interfacial interactions between analytes and functionalized sensor surfaces, from where the signal originates, is key to the development and application of electronic sensors. The present work explores the tunability of pH sensitivity by the synergy of surface charge and molecular dipole moment induced by interfacial proton interactions. This synergy is demonstrated on a silicon‐nanoribbon field‐effect transistor (SiNR‐FET) by functionalizing the sensor surface with properly designed chromophore molecules. The chromophore molecules can interact with protons and lead to appreciable changes in interface dipole moment as well as in surface charge state. In addition, the dipole moment can be tuned not only by the substituent on the chromophore but also by the anion in the electrolyte interacting with the protonated chromophore. By designing surface molecules to enhance the surface dipole moment upon protonation, an above‐Nernstian pH sensitivity is achieved on the SiNR‐FET sensor. This finding may bring an innovative strategy for tailoring the sensitivity of the SiNR‐FET‐based pH sensor toward a wide range of applications.
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| 9. |
- Wang, Longwei, et al.
(författare)
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Construction of S-N-C bond for boosting bacteria-killing by synergistic effect of photocatalysis and nanozyme
- 2023
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Ingår i: Applied Catalysis B: Environmental. - : Elsevier BV. - 0926-3373 .- 1873-3883. ; 325
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Tidskriftsartikel (refereegranskat)abstract
- Bacterial infection-related diseases are major public safety issues leads to millions of deaths annually. Herein, a porous sulfur doped graphitic carbon nitride (g-SCN) for ecofriendly, metal-free and low systemic toxicity were synthesized. Sulfur doping enables to broaden the absorption spectrum and promote the photocarriers separation for photocatalysis enhancement. Moreover, sulfur element will coordinate with nitrogen, changing the electronic state and endowing g-SCN with the property of nanozyme. More importantly, we established different models and confirmed that S-N-C coordination is the source of peroxidase (POD)-like activity through theory and experiment. The increased specific surface area of g-SCN, ascribing to the porous structure, makes it easier to trap bacteria. With the synergistic effect of photocatalysis and nanozyme, the prepared g-SCN has the ability to kill both gram-negative and gram-positive bacterium, with an antibacterial efficiency up to 100%. This work provides innovative synergistic strategy for constructing nanomaterials for highly efficient antibacterial therapy.
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