Prognostic value of creatine kinase (CK)-MB to total-CK ratio in colorectal cancer patients after curative resection.

OBJECTIVES: This study aimed to evaluate the prognostic significance of postoperative Creatine Kinase type M and B (CK-MB) to total Creatine Kinase (CK) ratio (CK-MB/CK) in colorectal cancer (CRC) patients after radical resection. METHODS: This was a single-center retrospective cohort analysis. Subjects were stage I-III CRC patients hospitalized in Sichuan Cancer Hospital from January 2017 to May 2021. Patients were divided into abnormal group and normal group according to whether the CK-MB/CK ratio was abnormal after surgery. Through a comparative analysis of clinical data, laboratory test results, and prognosis differences between the two groups, we aimed to uncover the potential relationship between abnormal CK-MB > CK results and CRC patients. To gauge the impact of CK-MB/CK on overall survival (OS) and disease-free survival (DFS), we employed the multivariable COX regression and LASSO regression analysis. Additionally, Spearman correlation analysis, logistic regression, and receiver-operating characteristic (ROC) curve analysis were conducted to assess the predictive value of the CK-MB/CK ratio for postoperative liver metastasis. RESULTS: Cox regression analysis revealed that the CK-MB/CK ratio was a stable risk factors for OS (HR = 3.82, p < 0.001) and DFS (HR = 2.31, p < 0.001). To distinguish hepatic metastases after surgery, the ROC area under the curve of CK-MB/CK was 0.697 (p < 0.001), and the optimal cut-off value determined by the Youden index was 0.347. CONCLUSIONS: Postoperative abnormal CK-MB/CK ratio predicts worse prognosis in CRC patients after radical resection and serves as a useful biomarker for detecting postoperative liver metastasis.

Higher cortical excitability to negative emotions involved in musculoskeletal pain in Parkinson's disease.

OBJECTIVE: Changes in brain structure and neurotransmitter systems are involved in pain in Parkinson's disease (PD), and emotional factors are closely related to pain. Our study applied electroencephalography (EEG) to investigate the role of emotion in PD patients with chronic musculoskeletal pain. METHODS: Forty-two PD patients with chronic musculoskeletal pain and 38 without were enrolled. EEG data were recorded under resting conditions, and while viewing pictures with neutral, positive, and negative content. We compared spectrum power, functional connectivity, and late positive potential (LPP), an event-related potential (ERP), between the groups. RESULTS: PD patients with pain tended to have higher scores for the Hamilton Rating Scale for Depression (HRSD). In the resting EEG, mean ß-band amplitude was significantly higher in patients with pain than in those without. Logistic regression analysis showed that higher HRSD scores and higher mean ß-band amplitude were associated with pain. ERP analysis revealed that the amplitudes of LPP difference waves (the absolute difference between positive and negative condition LPP and neutral condition LPP) at the central-parietal region were significantly reduced in patients with pain (P = 0.029). Spearman correlation analysis showed that the amplitudes of late (700-1000 ms) negative versus neutral condition LPP difference waves were negatively correlated with pain intensity, assessed by visual analogue scale, (r = -0.393, P = 0.010) and HRSD scores (r = -0.366, P = 0.017). CONCLUSION: Dopaminergic and non-dopaminergic systems may be involved in musculoskeletal pain in PD by increasing ß-band activity and weakening the connection of the θ-band at the central-parietal region. PD patients with musculoskeletal pain have higher cortical excitability to negative emotions. The changes in pain-related EEG may be used as electrophysiological markers and therapeutic targets in PD patients with chronic pain.

Hypermethylation of PPARG-encoding gene promoter mediates fine particulate matter-induced pulmonary fibrosis by regulating the HMGB1/NLRP3 axis.

The inflammatory response induced by fine particulate matter (PM2.5), a common class of air pollutants, is an important trigger for the development of pulmonary fibrosis. However, the specific mechanisms responsible for this phenomenon are yet to be fully understood. To investigate the mechanisms behind the onset and progression of lung fibrosis owing to PM2.5 exposure, both rats and human bronchial epithelial cells were subjected to varying concentrations of PM2.5. The involvement of the PPARG/HMGB1/NLRP3 signaling pathway in developing lung fibrosis caused by PM2.5 was validated through the utilization of a PPARG agonist (rosiglitazone), a PPARG inhibitor (GW9662), and an HMGB1 inhibitor (glycyrrhizin). These outcomes highlighted the downregulation of PPARG expression and activation of the HMGB1/NLRP3 signaling pathway triggered by PM2.5, thereby eliciting inflammatory responses and promoting pulmonary fibrosis. Additionally, PM2.5 exposure-induced DNA hypermethylation of PPARG-encoding gene promoter downregulated PPARG expression. Moreover, the DNA methyltransferase inhibitor 5-azacytidine mitigated the hypermethylation of the PPARG-encoding gene promoter triggered by PM2.5. In conclusion, the HMGB1/NLRP3 signaling pathway was activated in pulmonary fibrosis triggered by PM2.5 through the hypermethylation of the PPARG-encoding gene promoter.

How sleep quality affects activities of daily living in Parkinson's disease: the mediating role of disease severity and the moderating role of cognition.

Objective: The aim of this study was to explore the influential mechanism of the relationship between sleep quality and activities of daily living (ADL) in patients with Parkinson's disease (PD), we hypothesized disease severity as a mediator and assumed the mediating process was regulated by cognition. Methods: 194 individuals with PD (95 women and 99 men) were enrolled in study. The Pittsburgh Sleep Quality Index (PSQI) was used to assess sleep quality of PD patients. Patients' ADL, disease severity and cognition were measured by the Unified Parkinson's Disease Rating Scale-II (UPDRSII), Hoehn-Yahr (H-Y) Scale, and Mini-Mental State Examination (MMSE). We investigated the mediating role of disease severity and the moderating effect of cognition on the association between sleep quality and ADL in PD patients. Results: The score of UPDRSII was positively correlated with the score of PSQI and H-Y stage, while the score of MMSE was negatively correlated with the score of H-Y stage and UPDRSII. Sleep quality predicts disease severity, and disease severity predicts ADL. Disease severity mediated the relationship between sleep quality and ADL, and the mediating effect was 0.179. Cognition alone did not affect ADL, but the interaction between disease severity and cognition was significantly affected ADL, confirming the moderating effect of cognition in PD patients. Conclusion: Disease severity mediated the association between sleep quality and ADL, good cognition significantly reduced disease severity's mediating influence on the relationship between sleep quality and ADL. Our study indicated a close relationship between ADL and sleep and cognition in PD, and also provided new insights into the overall management of PD and a better quality of life of PD patients.

LINC01268 promotes epithelial-mesenchymal transition, invasion and metastasis of gastric cancer via the PI3K/Akt signaling pathway and targeting MARCKS.

BACKGROUND: Long non-coding RNAs (lncRNAs) with differential expression characteristics have been found to be closely related to the tumorigenesis and development of gastric cancer (GC), but their specific mechanisms and roles still need to be further elucidated. AIM: To investigate the expression of LINC01268 in GC and its mechanism of affecting GC progression. METHODS: Real-time quantitative polymerase chain reaction was used to detect the expression of LINC01268 in GC tissues, cell lines and plasma. The Kaplan-Meier method was used to evaluate the value of LINC01268 in the prognostication of GC patients. An receiver operating characteristic curve was constructed to evaluate the value of LINC01268 in the diagnosis of GC. Transwell migration and invasion assays and wound healing assays were used to confirm the effect of LINC01268 on the invasion and migration of GC cells. The regulatory relationship between LINC01268 and myristoylated alanine rich protein kinase C substrate (MARCKS), the PI3K/Akt signaling pathway, and the epithelial-mesenchymal transition (EMT) process in GC was demonstrated by western blot analysis. RESULTS: The expression of LINC01268 was increased in GC tissues and cell lines. The expression level of LINC01268 was significantly correlated with lymph node metastasis, TNM stage, and tumor differentiation in patients with GC. Over-expression of LINC01268 indicated a poor prognosis for patients with GC, and it had a certain auxiliary diagnostic value for GC. In vitro functional experiments proved that the abnormal expression of LINC01268 further activated the PI3K/Akt signaling pathway and promoted EMT by targeting and regulating MARCKS and ultimately promoted the invasion and metastasis of GC. CONCLUSION: This study elucidates that LINC01268 in GC may be an oncogene that further activates the PI3K/Akt signaling pathway and EMT by targeting and regulating MARCKS, and ultimately promotes the invasion and metastasis of GC. LINC01268 may be a potential effective target for the treatment of GC.

Pairing comparative genomics with tandem mass-based molecular networking allows to highly efficient discovery of nonribosomal peptides from Nocardia spp.

Microbial natural products, particularly nonribosomal peptides (NRPs), have attracted significant attention due to their structural diversity and therapeutic potential. Nocardia, a genus of Actinomyces, is an important reservoir for natural products, especially NRPs. However, rediscovery is a significant challenge for mining new specialized metabolites from Nocardia, as well as from other sources. To overcome this challenge, we developed a strategy that combines comparative genomics with tandem mass-based molecular networking, which allows to efficiently discover new NRPs from Nocardia spp.. As a proof of concept, all genomes of Norcardia in NCBI database, including three strains from our lab, were compared with each other to prioritize unique biosynthetic gene clusters (BGCs) in the three in-house Nocardia strains, particularly those containing nonribosomal peptide synthases (NRPSs). Subsequently, the metabolomics data of those three in-house strains were analyzed employing tandem mass-based molecular networking. This led to the identification of a known lipopeptide, nocarjamide (1), and five new congeners (2-6) of nocarjamide, as well as a new decalipopeptide, nocarlipoamide (7), along with nocardimicin, a known compound found in Nocardia. The structure of the new decalipopeptide 7 was further extensively characterized using NMR, MS/MS, Marfey's analysis, and X-ray. In addition, the biosynthesis pathways for 1-7 were proposed through bioinformatics analysis, and thus the gene clusters responsible for biosynthesizing them were confirmed. Our results indicate that this strategy enables prompt dereplication of known compounds, rapid linkage of identified compounds with their biosynthesis gene cluster, and efficient discovery of new compounds.

Nocaviogua A and B: two lipolanthines from root-nodule-associated Nocardia sp.

Nocaviogua A (1) and B (2), two lipolanthines featuring a non-canonical avionin (Avi)-containing macrocycle and a long acyl chain, were identified from the mutualistic actinomycete Nocardia sp. XZ19_369, which was isolated from the nodules of sea buckthorn collected in Tibet. Their planar structures were elucidated via extensive analyses of 1D and 2D NMR, as well as HRMS data. The absolute configurations were fully elucidated by advanced Marfey's analysis and GIAO NMR calculations, representing the first time that the configurations of this family of lipolanthines have been determined. Nocaviogua A (1) exhibited weak cytotoxicity against human chronic uveal melanoma cells (UM92-1), non-small cell lung cancer (NCI-H2170), and breast cancer (MDA-MB-231). Our work provides valuable information on this burgeoning class of lipolanthines for further investigations.

Insights of microalgal municipal wastewater treatment at low temperatures: Performance, microbiota patterns, and cold-adaptation of tubular and aeration column photobioreactors.

In order to refine the treatment of microalgae consortium (MC) for municipal wastewater (MWW) during the winter, this study investigated the effectiveness of tubular and aeration column photobioreactors (TPBR and APBR) in wastewater treatment plant (WWTP) during winter by two start-up modes: microalgae/microalgae-activated sludge (AS). The operation results showed that under 5.7-13.1 °C, TPBR enhanced the assimilation of N and P pollutant by microalgal accumulation, meeting the Chinese discharge standard within 24 h (NH4+-N, TP, and COD ≤8.0, 0.5, and 50 mg·L-1). The microbial community profiles were identified and showed that inoculating AS under low-temperature still promoted bacterial interspecific association, but influenced by the inhibition of microbial diversity by the homogeneous circulation of TPBR, the nitrogen transfer function of MC was lower than that of APBR at low temperatures, except nitrogen fixation (K02588), nitrosification (K10944, K10945, and K10946), assimilatory nitrate reduction (K00366), and ammonification (K01915 and K05601). And the intermittent aeration in the APBR was still beneficial in increasing microbial diversity, which was more beneficial for reducing COD through microbial collaboration. In the treatment, the cryotolerant MGPM were Delftia, Romboutsia, Rhizobiales, and Bacillus, and the cold stress-related genes that were highly up-regulated were defense signaling molecules (K03671 and K00384), cold shock protein gene (K03704), and cellular protector (K01784) were present in both PBRs. This study provided a reference for the feasibility of the low temperature treatment of MC with the different types of PBR, which improved the application of wastewater treatment in more climatic environments.

The association and prognostic value of systemic inflammatory response index with short and long-term mortality in patients with sepsis.

This study evaluated the association and prognostic significance of the systemic inflammation response index (SIRI) with mortality in sepsis. In this cohort study, the sepsis patients were retrieved from the Medical Information Mart for Intensive Care III (MIMIC-III) and MIMIC-IV intensive care unit (ICU) databases. SIRI was calculated by using the neutrophil, monocyte, and lymphocyte counts. The outcomes were 28-day mortality, 1-year mortality, and 28 days to 1-year mortality. The Cox proportional hazards model with a hazard ratio (HR) and a 95% confidence interval (CI) was used to investigate the association and prognostic value of SIRI with mortality in sepsis. Subgroup analyses of the associations of SIRI with 28-day and 1-year mortality in sepsis were based on age, gender, Simplified Acute Physiology Score II (SAPSII), Sequential Organ Failure Assessment (SOFA), and presence or absence of septic shock. The receiver operating characteristic (ROC) curve was used to compare the predictive performances of SIRI, SOFA and SAPS II for mortality in sepsis. Of the 4239 patients included, 1339 patients suffered from 28-day mortality, 2085 patients suffering from 1-year mortality, and 746 (25.72%) suffered from 28 days to 1-year mortality. High SIRI levels exhibited higher risks of 28-day mortality (HR: 1.15, 95% CI: 1.03-1.29, P = .010), 1-year mortality (HR: 1.14, 95% CI: 1.04-1.24, P = .003), and 28 days to 1-year mortality (HR: 1.16, 95% CI: 1.01-1.35, P = .047) in sepsis. A higher SIRI was reported related to 28-day mortality and 1-year mortality in sepsis patients with female gender, with SOFA < 8, with SAPS II < 44, and in sepsis patients without sepsis shock. The AUC of SIRS, SOFA, and SAPS II in predicting 28-day mortality in sepsis were 0.726, 0.591, and 0.644, respectively. The AUC of SIRI in predicting 1-year mortality in sepsis was 0.761, higher than the AUC values of SOFA and SAPS II. A higher AUC value of SIRI compared with SOFA, and SAPS II in predicting 28 days to 1-year mortality was observed. Elevated SIRI was associated with an increased risk of mortality in sepsis. SIRI is an independent prognostic biomarker of mortality in sepsis.

Synthesis of temperature- and humidity-induced dual stimulation film PU-PNIPAm n and its independent film formation as a smart window application.

Dynamic windows, which switch between transparent and opaque states as the temperature changes, can be applied in buildings to reduce building energy consumption. Poly(N-isopropylacrylamide) (PNIPAm) is the most studied thermochromic hydrogel for climate-resilient smart window applications. In addition to its poor mechanical properties and low reaction rate, the PNIPAm hydrogel must be sandwiched between two pieces of glass to form an interlayer in practical applications. Here, durable PU-PNIPAm n copolymers for smart windows were synthesized by reacting the synthesized poly-NIPAm diols with isocyanate (-NCO) monomer, which greatly improved the mechanical properties of the hydrogel and it was able to form a film alone. These temperature-sensitive films can switch between transparent (>80% transmittance) and opaque (<5% transmittance) states in less than 10 minutes, with no degradation in optical contrast, switching speed, or uniformity after at least 100 switching cycles.

High-Strength Ductility Joining of Multicomponent Alloy to 304 Stainless Steel Using Laser Welding Technique.

In this work, a series of multicomponent alloys (CoCrFeNi, CoCrNi, and CoNiV) were laser welded with 304 stainless steel (304ss), and detailed comparisons on microstructural characteristics and mechanical properties were conducted for dissimilar laser welded joints. It is revealed that all of the dissimilar laser welded samples possessed defect-free joints and the corresponding fusion zone consisting of fcc single-phase showed homogeneous element distribution accompanied by a narrow element gradient in the vicinity of the fusion zone boundary. After laser welding with identical welding parameters, equiaxed grain was observed on the side of multicomponent alloy, while coarse columnar grain was obtained on the side of 304ss. Especially, the columnar grains of the fusion zone on the side of 304ss disclosed preferential <001> growth direction in the CoCrFeNi/304ss and CoCrNi/304ss welded joints. Furthermore, all of the dissimilar laser welded joints were fractured in the fusion zone, attributing to the drastic loss of strength in the fusion zone with coarsened grain. It is worth noting that a special lamellar structure that merged by dimples was found in the fracture surface of the CoNiV/304ss joint, closely related to the existence of the V-enriched region. Finally, a high strength-ductile synergy can be achieved by laser welding CoNiV alloy to 304ss, which showed a yield strength of 338 MPa, ultimate tensile strength of 686 MPa, and total elongation of 28.9%. These excellent mechanical properties prevailed in the potential of a CoNiV/304ss laser welded joint to be applied as a structural material.

Myocardin-related transcription factor A, regulated by serum response factor, contributes to diabetic cardiomyopathy in mice.

AIMS: Diabetic cardiomyopathy is a significant contributor to the global pandemic of heart failure. In the present study we investigated the involvement of myocardin-related transcription factor A (MRTF-A), a transcriptional regulator, in this process. MATERIALS AND METHODS: Diabetic cardiomyopathy was induced in mice by feeding with a high-fat diet (HFD) or streptozotocin (STZ) injection. KEY FINDINGS: We report that MRTF-A was up-regulated in the hearts of mice with diabetic cardiomyopathy. MRTF-A expression was also up-regulated by treatment with palmitate in cultured cardiomyocytes in vitro. Mechanistically, serum response factor (SRF) bound to the MRTF-A gene promoter and activated MRTF-A transcription in response to pro-diabetic stimuli. Knockdown of SRF abrogated MRTF-A induction in cardiomyocytes treated with palmitate. When cardiomyocytes conditional MRTF-A knockout mice (MRTF-A CKO) and wild type (WT) mice were placed on an HFD to induce diabetic cardiomyopathy, it was found that the CKO mice and the WT mice displayed comparable metabolic parameters including body weight, blood insulin concentration, blood cholesterol concentration, and glucose tolerance. However, both systolic and diastolic cardiac function were exacerbated by MRTF-A deletion in the heart. SIGNIFICANCE: These data suggest that MRTF-A up-regulation might serve as an important compensatory mechanism to safeguard the deterioration of cardiac function during diabetic cardiomyopathy.

Vitamin B complex blocks the dust fall PM2 .5 -induced acute lung injury through DNA methylation in rats.

This study aimed to explore whether vitamin B complex (folic acid, B6 , and B12 ) could avert DNA methylation changes associated with inflammation induced by acute PM2.5 exposure. Sprague-Dawley rats were administered by gavage with different concentrations of vitamin B complex once a day for 28 days, and then by intratracheal instillation with saline or PM2.5 once every 2 days for three times. Vitamin B continued to be taken during the PM2.5 exposure. Rats were sacrificed 24 h after the last exposure. The results showed that vitamin B complex could block the pathological changes and injury in lungs induced by PM2.5 . Meanwhile, vitamin B complex could prevent the abnormal DNA methylation of IL-4 and IFN-γ to antagonize the imbalance of IL-4/IFN-γ associated with inflammation. It was further found that vitamin B complex could regulate DNA methyltransferases (DNMTs) and increase the S-adenosylmethionine (SAM)/S-Adenosyl-L-homocysteine (SAH) ratio to reverse the hypomethylation of genomic DNA and the abnormal DNA methylation of IL-4 and IFN-γ. In conclusion, vitamin B complex has a protective effect on acute lung injury by attenuating abnormal DNA methylation induced by PM2.5 in rats. This study may provide a new insight into the physiological function of vitamin B to prevent the health effects induced by PM2.5 .

Multiferroic and Magnetodielectric Effects in Multiferroic Pr2FeAlO6 Double Perovskite.

Single-phase multiferroics that allow the coexistence of ferroelectric and magnetic ordering above room temperature are highly desirable, and offer a fundamental platform for novel functionality. In this work, a double perovskite multiferroic Pr2FeAlO6 ceramic is prepared using a sol-gel process followed by a quenching treatment. The well-crystallized and purified Pr2FeAlO6 in trigonal structure with space group R3c is confirmed. A combination of the ferroelectric (2Pr = 0.84 µC/cm2, Ec = 7.78 kV/cm at an applied electric field of 20 kV/cm) and magnetic (2Mr = 433 memu/g, Hc = 3.3 kOe at an applied magnetic field of 1.0 T) hysteresis loops reveals the room-temperature multiferroic properties. Further, the magnetoelectric effect is observed from the measurements of magnetically induced dielectric response and polarization. The present results suggest a new complex oxide candidate for room-temperature multiferroic applications.

Functional role of the SLC7A11-AS1/xCT axis in the development of gastric cancer cisplatin-resistance by a GSH-dependent mechanism.

Resistance to platinum-based chemotherapy is a major obstacle in gastric cancer (GC) treatment. Abundant long noncoding RNAs (lncRNAs) are reported to play important roles in tumorigenesis and drug resistance biology. Herein, we report that the SLC7A11-AS1 and xCT are involved in cisplatin resistance in GC. SLC7A11-AS1 was downregulated and xCT was upregulated in cisplatin-resistant GC tissues and cell lines. GC patients with low expression of SLC7A11-AS1 and high expression of xCT had a poor prognosis and relatively poor response to chemotherapy. Overexpression of SLC7A11-AS1 weakened GC growth, reduced intracellular GSH biosynthesis, enhanced intracellular reactive oxygen species (ROS) and conferred sensitivity to cisplatin to resistant GC cells in vitro and in vivo. Mechanistically, SLC7A11-AS1 directly suppressed xCT expression, while miR-33a-5p remarkably reduced SLC7A11-AS1 and xCT expression by directly targeting the SLC7A11-AS1 and xCT 3'UTRs. In addition, we found that low SLC7A11-AS1 expression activated the p38MAPK-JNK signaling pathway, and increased the expression of cisplatin export gene ATP7A and the GSH biosynthesis gene GCLM in GC.

An analysis of risk factors for carbapenem-resistant Enterobacteriaceae infection.

OBJECTIVES: This study aims to explore the high-risk factors of carbapenem-resistant Enterobacteriaceae (CRE) infection of hospitalised patients in high-risk departments. METHODS: This study is a multicentre, retrospective study. CRE screening positive patients from 1 January 2016 to 31 December 2018 of high-risk departments in five tertiary first-class teaching hospitals in Beijing collect the patients' CRE test specimen information, CRE infection information and outcomes. The patients were divided into a colonisation group and an infection group for comparative analysis. A logistic regression model was established to explore the risk factors of CRE infection. Subgroup analysis was conducted according to invasive procedures and the type of the infection. RESULTS: In total, 344 patients were included in this study, including 85 (24.71%) colonisation and 259 (75.29%) infection; 36.09% CRE colonisation converted to infection, and the mean conversion time from colonisation to infection was 6.5 (4.0, 18.8) days. Renal disease, granulocytosis, invasive procedures and the time from hospital stay to positive CRE were the risk factors for CRE infection. The subgroup analysis showed that the rate of CRE infection in the invasive group was higher than in the non-invasive group (P < 0.001), and the rate of exacerbation or death in the invasive group was also higher than in the non-invasive group (P = 0.019). The average length of ICU and hospitalisation in the healthcare-associated infection group were significantly higher than those in the community infection group, but there was no difference in the proportion of final exacerbation or death between them (P = 0.727). CONCLUSION: Kidney disease, granulocytosis, invasive procedures and CRE detection time are the risk factors for CRE infection. Carrying out CRE screening in patients as early as possible and taking effective intervention measures in time to avoid adverse consequences is all important.

Long noncoding RNA LINC01606 protects colon cancer cells from ferroptotic cell death and promotes stemness by SCD1-Wnt/ß-catenin-TFE3 feedback loop signalling.

BACKGROUND: Ferroptosis is principally caused by iron catalytic activity and intracellular lipid peroxidation. Long noncoding RNAs (lncRNAs) play crucial roles in tumorigenesis. However, the potential interplay between lncRNA LINC01606 and ferroptosis in colon cancer remains elusive. METHODS: The expression level of LNC01606 in colon cancer tissue was detected by quantitative real-time polymerase chain reaction. The functional role of LNC01606 was investigated by gain- and loss-of-function assays both in vitro and in vivo. The LINC01606-SCD1-Wnt/ß-catenin-TFE3 axis were screened and validated by DNA/RNA pull down, gas chromatography-mass spectrometry, RNA immunoprecipitation and dual-luciferase reporter. RESULTS: The expression of lncRNA LINC01606 was frequently upregulated in human colon cancer and strongly associated with a poor prognosis. LINC01606 functioned as an oncogene and promotes colon cancer cell growth, invasion and stemness both in vitro and in vivo. Moreover, LINC01606 protected colon cancer cells from ferroptosis by decreasing the concentration of iron, lipid reactive oxygen species, mitochondrial superoxide and increasing mitochondrial membrane potential. Mechanistically, LINC01606 enhanced the expression of stearoyl-CoA desaturase 1 (SCD1), serving as a competing endogenous RNA to modulate miR-423-5p expression, subsequently activating the canonical Wnt/ß-catenin signaling, and transcription factor binding to IGHM enhancer 3 (TFE3) increased LINC01606 transcription after recruitment to the promoter regions of LINC01606. Furthermore, we confirmed that upregulated LINC01606 and Wnt/ß-catenin formed a positive feedback regulatory loop, further inhibiting ferroptosis and enhancing stemness. CONCLUSIONS: LINC01606 functions as an oncogene to facilitate tumor cell stemness, proliferation and inhibit ferroptosis and is a promising therapeutic target for colon cancer.