Destruxin B Suppresses Drug-Resistant Colon Tumorigenesis and Stemness Is Associated with the Upregulation of miR-214 and Downregulation of mTOR/β-Catenin Pathway

Wu, Szu-Yuan; Huang, Yan; Tzeng, Yew Min; Huang, Chi Ying F.; Hsiao, Michael; Wu, Alexander T.H.; Huang, Tse-Hung

doi:10.3390/cancers10100353

Cited by 15 publications

(7 citation statements)

References 35 publications

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“…It has been reported that the mTOR signaling pathway can induce colon cancer tumorigenesis (29). Furthermore, several studies have showed that antitumor effects can be enhanced by inhibiting mTOR signaling pathway in colon cancer cells (30,31). Similarly, our results showed that Shikonin induced colon cancer cell apoptosis by down-regulating activation of mTOR signaling.…”

Section: Discussionsupporting

confidence: 76%

Shikonin-induced Apoptosis of Colon Cancer Cells Is Reduced by Peroxiredoxin V Expression

et al. 2019

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Background/Aim: Colon cancer is the second most common deadliest malignancy in the world and better understanding of its underlying mechanisms is needed to improve clinical management. Natural plant extracts are gaining attention in the development of new therapeutic strategies against various cancer types. Shikonin is a naturally extracted naphthoquinone pigment with effects against cancer, including colon cancer. Materials and Methods: In this study, we conducted a series of in vitro experiments to show the effects of Shikonin on colon cancer cell apoptosis. A colon cancer cell line with overexpression of peroxiredoxin V (PrxV) was constructed and the relationship of PrxV expression with Shikonin-induced cell apoptosis was investigated. Results: Shikonin induced colon cancer cell apoptosis via regulation of mammalian target of rapamycin signaling. Shikonin-induced cell apoptosis was abrogated by overexpression of PrxV. Conclusion: According to the results obtained in this study, targeting PrxV may provide new insight for the successful management of colon cancer by inducing cell apoptosis.

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Section: Discussionsupporting

confidence: 76%

Shikonin-induced Apoptosis of Colon Cancer Cells Is Reduced by Peroxiredoxin V Expression

et al. 2019

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“…We conducted a population-based cohort study using Taiwan National Health Insurance (NHI) Research Data (NHIRD) linked to the TCRD. The TCRD was established in 1979 and contains 97% of the cancer cases in Taiwan [ 13 ]. The NHIRD includes all medical claims data on disease diagnoses, procedures, drug prescriptions, demographics, and enrollment profiles of all beneficiaries [ 14 ].…”

Section: Methodsmentioning

confidence: 99%

There Are No Differences in Positive Surgical Margin Rates or Biochemical Failure–Free Survival among Patients Receiving Open, Laparoscopic, or Robotic Radical Prostatectomy: A Nationwide Cohort Study from the National Cancer Database

Chang

Chen

2020

Cancers

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Purpose: To estimate the rates of positive surgical margin (PSM) and biochemical failure–free survival (BFS) among patients with prostate cancer (PC) receiving open, laparoscopic, or robotic radical prostatectomy (RP). Patients and Methods: The patients were men enrolled in the Taiwan Cancer Registry diagnosed as having PC without distant metastasis who received RP. After adjustment for confounders, logistic regression was used to model the risk of PSM following RP. After adjustment for confounders, Cox proportional regression was used to model the time from the index (i.e., surgical) date to biochemical recurrence. Results: The adjusted odds ratios (95% CIs) of PSM risk after propensity score adjustment for laparoscopic versus open, robotic versus open, and robotic versus laparoscopic RP 95% CIs were 1.25 (0.88 to 1.77; p = 0.2064), 1.16 (0.88 to 1.53; p = 0.2847), and 0.93 (0.70 to 1.24; p = 0.6185), respectively. The corresponding adjusted hazard ratios (95% CIs) of risk of biochemical failure after propensity score adjustment were 1.16 (0.93 to 1.47; p = 0.1940), 1.10 (0.83 to 1.47; p = 0.5085), and 0.95 (0.74 to 1.21; p = 0.6582). Conclusions: No significant differences in PSM or BFS were observed among patients receiving open, laparoscopic, or robotic RP.

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“…miR-214 was frequently reported to be a tumor suppressive miRNA ( Wu et al, 2018 ; Karimkhanloo et al, 2020 ). Here, we found that SPINT1-AS1 and miR-214 reciprocally repressed each other.…”

Section: Resultsmentioning

confidence: 99%

“…The critical oncogenic protein β-catenin was a well-known miR-214 downstream target ( Wu et al, 2018 ; Karimkhanloo et al, 2020 ). Given that SPINT1-AS1 exerts oncogenic roles in cervical cancer via binding DNM3OS and repressing miR-214 biogenesis, we further explored the potential roles of SPINT1-AS1 on Wnt/β-catenin signaling.…”

Section: Resultsmentioning

confidence: 99%

SPINT1-AS1 Drives Cervical Cancer Progression via Repressing miR-214 Biogenesis

Song

Liu

Liang

et al. 2021

Front. Cell Dev. Biol.

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Accumulating evidences have revealed the dysregulated expressions and critical roles of non-coding RNAs in various malignancies, including cervical cancer. Nevertheless, our knowledge about the vast majority of non-coding RNAs is still lacking. Here we identified long non-coding RNA (lncRNA) SPINT1-AS1 as a novel cervical cancer-associated lncRNA. SPINT1-AS1 was increased in cervical cancer and correlated with advanced stage and poor prognosis. SPINT1-AS1 was a direct downstream target of miR-214, a well-known tumor suppressive microRNA (miRNA) in cervical cancer. Intriguingly, SPINT1-AS1 was also found to repress miR-214 biogenesis via binding DNM3OS, the primary transcript of miR-214. The interaction between SPINT1-AS1 and DNM3OS repressed the binding of DROSHA and DGCR8 to DNM3OS, blocked DNM3OS cleavage, and therefore repressed mature miR-214 biogenesis. The expression of SPINT1-AS1 was significantly negatively correlated with miR-214 in cervical cancer tissues, supporting the reciprocal repression between SPINT1-AS1 and miR-214 in vivo. Through downregulating mature miR-214 level, SPINT1-AS1 upregulated the expression of β-catenin, a target of miR-214. Thus, SPINT1-AS1 further activated Wnt/β-catenin signaling in cervical cancer. Functionally, SPINT1-AS1 drove cervical cancer cellular proliferation, migration, and invasion in vitro, and also tumorigenesis in vivo. Deletion of the region mediating the interaction between SPINT1-AS1 and DNM3OS, overexpression of miR-214, and inhibition of Wnt/β-catenin signaling all reversed the roles of SPINT1-AS1 in cervical cancer. Collectively, these findings identified SPINT1-AS1 as a novel cervical cancer-associated oncogenic lncRNA which represses miR-214 biogenesis and activates Wnt/β-catenin signaling, highlighting its potential as prognostic biomarker and therapeutic target for cervical cancer.

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Destruxin B Suppresses Drug-Resistant Colon Tumorigenesis and Stemness Is Associated with the Upregulation of miR-214 and Downregulation of mTOR/β-Catenin Pathway

Cited by 15 publications

References 35 publications

Shikonin-induced Apoptosis of Colon Cancer Cells Is Reduced by Peroxiredoxin V Expression

Shikonin-induced Apoptosis of Colon Cancer Cells Is Reduced by Peroxiredoxin V Expression

There Are No Differences in Positive Surgical Margin Rates or Biochemical Failure–Free Survival among Patients Receiving Open, Laparoscopic, or Robotic Radical Prostatectomy: A Nationwide Cohort Study from the National Cancer Database

SPINT1-AS1 Drives Cervical Cancer Progression via Repressing miR-214 Biogenesis

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