The autophagic inhibition oral squamous cell carcinoma cancer growth of 16-hydroxy-cleroda-3,14-dine-15,16-olide

Cheng, Ming‐Fang; Lin, Shian-Ren; Tseng, Fong-Jen; Huang, Yo-Ping; Tsai, Ming-Tzu; Fu, Yaw-Syan; Weng, Ching‐Feng

doi:10.18632/oncotarget.18987

Cited by 18 publications

(28 citation statements)

References 65 publications

(70 reference statements)

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“…In our previous study, HCD was demonstrated to be a non-toxic agent to normal cells [16]. When compared to 5-FU, the cytotoxicity of HCD against colorectal cancer was higher than 5-FU (4.10 vs. 100 µM in IC 50 at 36 h treatment), suggesting that HCD had higher efficacy and more potent when applied to colon cancer treatments.…”

Section: Discussionmentioning

confidence: 95%

“…injected once every three days until day 65. Mice were sacrificed by CO 2 anesthesia, and their colons were collected for slicing in the literature [16].…”

Section: Inflammatory Bowel Disease Model Induction and Hcd Treatmentmentioning

confidence: 99%

“…The cytotoxic effect of HCD was measured by MTT (3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide; MDBio Inc., Taipei City, Taiwan) assay, as previously described in the literature [16]. Briefly, 7 × 10 3 cells per well of two cells were inoculated in 96-well plates before incubating with 0.5, 2.0, 5.0, and 10.0 µM of HCD and 1, 10, 50, and 100 µM of 5-FU (a positive control) for 36 and 48 h, respectively.…”

Section: Cytotoxicity Assaymentioning

confidence: 99%

“…The protocol of cell cycle analysis followed a previous study, with slight modification [16]. In brief, 7 × 10 4 cells per well of Caco-2 cells were seeded into 12-well plates.…”

Section: Cell Cycle Analysismentioning

confidence: 99%

“…Cells were treated with 0.5, 1.0, and 2.0 µM of HCD for 24 and 36 h, respectively. After incubation, cells were homogenized, and the desired protein levels were analyzed according to the protocol described in a previous study [16]. The chemiluminometric intensity of each protein was normalized with GAPDH's chemiluminometric intensity.…”

Section: Western Blottingmentioning

confidence: 99%

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Clerodane Diterpene Ameliorates Inflammatory Bowel Disease and Potentiates Cell Apoptosis of Colorectal Cancer

et al. 2019

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Inflammatory bowel disease (IBD) is general term for ulcerative colitis and Crohn's disease, which is chronic intestinal and colorectal inflammation caused by microbial infiltration or immunocyte attack. IBD is not curable, and is highly susceptible to develop into colorectal cancer. Finding agents to alleviate these symptoms, as well as any progression of IBD, is a critical effort. This study evaluates the anti-inflammation and anti-tumor activity of 16-hydroxycleroda-3,13-dien-15,16-olide (HCD) in in vivo and in vitro assays. The result of an IBD mouse model induced using intraperitoneal chemical azoxymethane (AOM)/dextran sodium sulfate (DSS) injection showed that intraperitoneal HCD adminstration could ameliorate the inflammatory symptoms of IBD mice. In the in vitro assay, cytotoxic characteristics and retained signaling pathways of HCD treatment were analyzed by MTT assay, cell cycle analysis, and Western blotting. From cell viability determination, the IC 50 of HCD in Caco-2 was significantly lower in 2.30 µM at 48 h when compared to 5-fluorouracil (5-FU) (66.79 µM). By cell cycle and Western blotting analysis, the cell death characteristics of HCD treatment in Caco-2 exhibited the involvement of extrinsic and intrinsic pathways in cell death, for which intrinsic apoptosis was predominantly activated via the reduction in growth factor signaling. These potential treatments against colon cancer demonstrate that HCD could provide a promising adjuvant as an alternative medicine in combating colorectal cancer and IBD.

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Section: Discussionmentioning

confidence: 95%

“…injected once every three days until day 65. Mice were sacrificed by CO 2 anesthesia, and their colons were collected for slicing in the literature [16].…”

Section: Inflammatory Bowel Disease Model Induction and Hcd Treatmentmentioning

confidence: 99%

Section: Cytotoxicity Assaymentioning

confidence: 99%

“…The protocol of cell cycle analysis followed a previous study, with slight modification [16]. In brief, 7 × 10 4 cells per well of Caco-2 cells were seeded into 12-well plates.…”

Section: Cell Cycle Analysismentioning

confidence: 99%

Section: Western Blottingmentioning

confidence: 99%

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Clerodane Diterpene Ameliorates Inflammatory Bowel Disease and Potentiates Cell Apoptosis of Colorectal Cancer

et al. 2019

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Autophagy modulators for the treatment of oral and esophageal squamous cell carcinomas

Khan

Relitti

Brindisi

et al. 2019

Medicinal Research Reviews

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Oral squamous cell carcinomas (OSCC) and esophageal squamous cell carcinomas (ESCC) exhibit a survival rate of less than 60% and 40%, respectively. Late-stage diagnosis and lack of effective treatment strategies make both OSCC and ESCC a significant health burden. Autophagy, a lysosome-dependent catabolic process, involves the degradation of intracellular components to maintain cell homeostasis. Targeting autophagy has been highlighted as a feasible therapeutic strategy with clinical utility in cancer treatment, although its associated regulatory mechanisms remain elusive. The detection of relevant biomarkers in biological fluids has been anticipated to facilitate early diagnosis and/or prognosis for these tumors. In this context, recent studies have indicated the presence of specific proteins and small RNAs, detectable in circulating plasma and serum, as biomarkers. Interestingly, the interplay between biomarkers (eg, exosomal microRNAs) and autophagic processes could be exploited in the quest for targeted and more effective therapies for OSCC and ESCC. In this review, we give an overview of the available biomarkers and innovative targeted therapeutic strategies, including the application of autophagy modulators in OSCC and ESCC.Additionally, we provide a viewpoint on the state of the art Tuhina Khan and Nicola Relitti contributed equally to this work. and on future therapeutic perspectives combining the early detection of relevant biomarkers with drug discovery for the treatment of OSCC and ESCC. K E Y W O R D S autophagy, autophagy modulators, biomarkers, esophageal squamous cell carcinoma, exosomes, oral squamous cell carcinoma, targeted therapy 1 | INTRODUCTION Oral squamous cell carcinoma (OSCC) is the predominant malignant neoplasm of the oral cavity followed by verrucous carcinoma, undifferentiated carcinoma, and small salivary adenocarcinoma. 1 Esophageal squamous cell carcinoma (ESCC) is the first histological type and accounts for 80% of cases of esophageal cancer. 2 OSCC and ESCC are indicated as one of the most common cancers by the International Union Against Cancer with an annual incidence of 275 000 and 456 000 cases worldwide, respectively. 3,4 The primary etiology in both OSCC and ESCC is attributed to the environmental factors (tobacco abuse, alcohol consumption), genetic factors (eg, mutations in enzymes), viral factors (human papilloma virus [HPV] infection), and/or the coexistence of these factors. Alcohol intake and tobacco use are responsible for at least 75% of these carcinomas. The underlying initiation and progression mechanisms of OSCC and ESCC are generally characterized by the accumulation of serial epigenetic and genetic alterations, which eventually lead to uncontrolled proliferation of the mutated cells, followed by vigorous cell division. 5,7 Early-stage OSCC detection displays an 80% survival rate at 5 years, while detection at advanced stage leads to survival rates ranging from 20% to 40%. 6 In ESCC, the 5-year survival rate for early-stage detection may reach 85%, whereas a dr...

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Modulation of cancer stemness property in head and neck cancer cells via circulatory fluid shear stress

Goh

Pai

Cheng

et al. 2022

Microfluid Nanofluid

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The autophagic inhibition oral squamous cell carcinoma cancer growth of 16-hydroxy-cleroda-3,14-dine-15,16-olide

Cited by 18 publications

References 65 publications

Clerodane Diterpene Ameliorates Inflammatory Bowel Disease and Potentiates Cell Apoptosis of Colorectal Cancer

Clerodane Diterpene Ameliorates Inflammatory Bowel Disease and Potentiates Cell Apoptosis of Colorectal Cancer

Autophagy modulators for the treatment of oral and esophageal squamous cell carcinomas

Modulation of cancer stemness property in head and neck cancer cells via circulatory fluid shear stress

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