#hnok

[raineehavenday]

Honk

Honk

Moth honked at you.

Honk back or join the fray?

[some-murmurings]

slaughtered by fatigue today. rivers run red w/ our eepyness. my somnolent nature is a greater maw widening still. nap time

[roastedsoup]

my car

♥️hnok

[catalyticgenesis]

i made a friend. perhaps. or at least not a new enemy. good times in central park.

[misterbrick42]

hnok

honk if you are in the mood for some likes

[berdushbebe]

Yeni yerinde yine efso lezzetler ile @anteplimehmetusta2 (Antepli Mehmet Usta) https://www.instagram.com/p/B5GKTs-HNok/?igshid=vrvhnl66djyk

[afalloutassassin-blog]

hnok

Plez maek me famuss

[kamchronicles]

#TravisScott and his daughter #Stormie ❤️ https://www.instagram.com/p/By1xQz-HNok/?igshid=1b51334ggl3ae

[suspiciouslyglowingmoss]

HONK HoNK hNOK HOnkHONkHOMK HONK

I love when geese migrate for the winter because they just be making noise

[rnomics]

[Circular #RNA circHIPK3 acts as the sponge of #microRNA-124 to promote human oral squamous cell carcinoma cells proliferation].

Related Articles [Circular #RNA circHIPK3 acts as the sponge of #microRNA-124 to promote human oral squamous cell carcinoma cells proliferation]. Zhonghua Kou Qiang Yi Xue Za Zhi. 2018 Aug 09;53(8):546-551 Authors: Wang J, Zhao SY, Ouyang SS, Huang ZK, Luo Q, Liao L Abstract Objective: To explore the expression and clinical significance of circular #RNA circHIPK3 in oral squamous cell carcinoma (OSCC), analyze the effect of circHIPK3 on the proliferation of OSCC cells. Methods: The expression of circHIPK3 in OSCC tissues, adjacent non-#cancerous tissues and OSCC cell lines were detected by quantitative real-time polymerase chain reaction (qPCR). The correlations between the expression of circHIPK3 in OSCC tissues and the clinicopathological features were analyzed as well. circHIPK3-specific #siRNA si-circHIPK3 and negative control #siRNA si-NC were designed and synthesised and used to transfect CAL27 and SCC15 cells respectively. The proliferation capacity of CAL27 and SCC15 cells after transfection with si-circHIPK3 was detected by CCK-8 assay. The expression of miR-124 in OSCC was detected by qPCR, and the correlation between expression of circHIPK3 and the expression of miR-124 was analyzed. Using qPCR to detect the expression of miR-124 in CAL27 and SCC15 cells after transfection with si-circHIPK3 and si-NC respectively. Furthermore, using CCK-8 assay to detect the proliferation capacity of CAL27 and SCC15 cells after transfection with si-NC, si-circHIPK3, miR-124 mimic, si-circHIPK3+miR-124 inhibitor. Results: The expression of circHIPK3 in OSCC tissues [2.23 (1.86, 3.00)] was significantly higher than that of the adjacent non-#cancerous tissues [1.05 (0.85, 1.26)] (U=1 094, P=0.000). The expression of circHIPK3 in CAL27 (3.02±0.51) and SCC15 cells (3.16±0.75) was higher than those of human normal oral keratinocytes (hNOK) (1.26±0.30) (P=0.000). The expression of circHIPK3 was found to be closely associated with TNM stage (P http://bit.ly/2wtbYcz #Pubmed

[komaedalovemail]

Hnok

[hmcarchive-blog]

quak quak....

HNOK

[healthtimetaylor]

Licochalcone-E induces caspase-dependent death of human pharyngeal squamous carcinoma cells.

PMID:  Oncol Lett. 2017 May ;13(5):3662-3668. Epub 2017 Mar 16. PMID: 28521469 Abstract Title:  Licochalcone-E induces caspase-dependent death of human pharyngeal squamous carcinoma cells through the extrinsic and intrinsic apoptotic signaling pathways. Abstract:  The aim of the present study was to investigate licochalcone-E (Lico-E)-induced apoptosis and the associated apoptotic signaling pathway in FaDu cells, a human pharyngeal squamous carcinoma cell line. Treatment with Lico-E exhibited significant cytotoxicity on FaDu cells in a concentration-dependent manner. The ICvalue of Lico-E in FaDu cells was ~50µM. Treatment with Lico-E increased the number of dead FaDu cells. Furthermore, chromatin condensation, which is associated with apoptotic cell death, was observed in FaDu cells treated with Lico-E for 24 h. By contrast, Lico-E did not produce cytotoxicity or increase the number of dead cells whenapplied to human normal oral keratinocytes (hNOKs). Furthermore, chromatin condensation was not observed in hNOKs treated with Lico-E. Treatment with Lico-E increased the expression of Fas ligand and the cleaved form of caspase-8 in FaDu cells. Furthermore, treatment with Lico-E increased the expression of pro-apoptotic factors, including apoptosis regulator BAX, Bcl-2-associated agonist of cell death, apoptotic protease-activating factor 1, caspase-9 and tumor suppressor p53, while decreasing the expression of anti-apoptotic factors, including apoptosis regulator Bcl-2 and Bcl-2-like protein1 in FaDu cells. The expression of cleaved caspases-3 and poly (ADP-ribose) polymerase was significantly upregulated following treatment with Lico-E in FaDu cells, while Lico-E-induced apoptotic FaDu cell death was partially suppressed by treatment with Z-VAD-FMK, a pan caspase inhibitor. Therefore,Lico-E-induced oral cancer (OC) cell-specific apoptosis is mediated by the death receptor-dependent extrinsic and mitochondrial-dependent intrinsic apoptotic signaling pathways. In conclusion, these data suggested that Lico-E exhibits potential chemopreventive effects and warrants further developedas a chemotherapeutic agent against OC.

read more

[catalyticgenesis]

things that ive lost or otherwise abandoned since 2015: actual good grades, many friendships, hope for the future, my will to live, any art skills, the hope for a musical that wont make me want to kill myself, any remaining dignity, etc.

things that have somehow persisted, logic be damned, this shit will never fucking leave: my goddamn hnok tag i was in honk frESHMAN year i swear that musical has permanently altered my sense of humor

[cancersfakianakis1]

Transcriptome reprogramming by cancer exosomes: identification of novel molecular targets in matrix and immune modulation

Abstract

Background

Exosomes are extracellular vesicles released by almost all cell types, including cancer cells, into bodily fluids such as saliva, plasma, breast milk, semen, urine, cerebrospinal fluid, amniotic fluid, synovial fluid and sputum. Their key function being intercellular communication with both neighbouring as well as distant cells. Cancer exosomes have been shown to regulate organ-specific metastasis. However, little is known about the functional differences and molecular consequences of normal cells responding to exosomes derived from normal cells compared to those derived from cancer cells.

Methods

Here, we characterised and compared the transcriptome profiles of primary human normal oral keratinocytes (HNOK) in response to exosomes isolated from either primary HNOK or head and neck squamous cell carcinoma (HNSCC) cell lines.

Results

In recipient HNOK cells, we found that regardless of normal or cancer derived, exosomes altered molecular programmes involved in matrix modulation (MMP9), cytoskeletal remodelling (TUBB6, FEZ1, CCT6A), viral/dsRNA-induced interferon (OAS1, IFI6), anti-inflammatory (TSC22D3), deubiquitin (OTUD1), lipid metabolism and membrane trafficking (BBOX1, LRP11, RAB6A). Interestingly, cancer exosomes, but not normal exosomes, modulated expression of matrix remodelling (EFEMP1, DDK3, SPARC), cell cycle (EEF2K), membrane remodelling (LAMP2, SRPX), differentiation (SPRR2E), apoptosis (CTSC), transcription/translation (KLF6, PUS7). We have also identified CEP55 as a potential cancer exosomal marker.

Conclusions

In conclusion, both normal and cancer exosomes modulated unique gene expression pathways in normal recipient cells. Cancer cells may exploit exosomes to confer transcriptome reprogramming that leads to cancer-associated pathologies such as angiogenesis, immune evasion/modulation, cell fate alteration and metastasis. Molecular pathways and biomarkers identified in this study may be clinically exploitable for developing novel liquid-biopsy based diagnostics and immunotherapies.

https://ift.tt/2L8Psyl

[catalyticgenesis]

fuck geese