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Recently, bispecific antibodies (BsAbs) are evolving the landscape of cancer treatment and have significantly improved the outcomes of relapsed or refractory cancer patients. As increasing BsAbs entered clinical practice, specific toxicities have emerged, and renal side-effects have been described. However, there are a lack of studies analyzing the nephrotoxicity in the anti-cancer BsAbs recipients systematically. In this review, we demonstrate the etiologies, mechanisms, other risk factors and treatment options of kidney injury in the BsAbs recipients to provide a more comprehensive insight into the nephrotoxicity post-BsAbs therapy. Significantly, due to the limited clinical trial data on each subject, we mainly conclude the related etiologies, mechanisms, and risk factors of nephrotoxicity that occur in T-cell-engaging BsAbs recipients. Nephrotoxicity associated with non-T-cell BsAbs may be associated with adverse nephrotoxicity of related monoclonal antibodies to two specific antigens. The aim of this paper is to provide nephrologists and oncologists with theoretical knowledge to provide better medical management for recipients who receive BsAbs, especially T-cell-engaging BsAbs treatment. [ABSTRACT FROM AUTHOR]

Background: Primary pancreatic mucoepidermoid carcinoma (MEC) is an extremely rare malignant tumor with unclear etiology and pathogenesis. There are only eleven reported cases in English papers published from 1959 to 2020. MEC generally occurs in the salivary gland, but cases in the pancreas have also been reported. Although being considered as a low-grade indolent carcinoma, pancreatic MEC always invades the surrounding lymph node and metastasizes. The prognosis of pancreatic MEC is unsatisfactory. To date, the genetic alterations, mechanistic relationships among mutated genes and signaling pathways of pancreatic MEC are unclear. Patient and Methods: This paper presents a case of rare primary pancreatic MEC in a 56-year-old male patient with liver metastasis. Radical surgery of distal pancreatectomy and radiofrequency ablation (RFA) of two liver metastatic lesions is conducted. Targeted-gene sequencing and bioinformatics analysis tools, including STRING, DAVID, cBioPortal, DGidb and Human Protein Atlas database (HPA), are used to clarify the biological functions and features of mutated genes in pancreatic MEC. Results: Eight gene mutations (TP53, KRAS, ATR, FLI1, FLT4, MAGI2, RBM10, and TNFAIP3) were observed, and a tumor mutation burden (TMB) of 5.6 muts/Mb was calculated in the pancreatic MEC using targeted-gene sequencing. The patient subsequently underwent adjuvant chemotherapy and died three months after surgery. Gene–gene interaction network was constructed, which showed the significant interactions among eight mutated genes. In terms of the functions and pathways of eight gene mutations based on GO and KEGG, 20 tumor-related results are presented in this paper, Furthermore, the biological functions and features of pancreatic MEC are further compared with pancreatic ductal adenocarcinoma. Conclusion: Pancreatic MEC requires early and effective treatment, and lymph node metastases and multiple organ metastases were unfavorable prognostic factors. Pancreatic MEC can be compared with other pancreatic cancers that have characteristic clinical phenotype, molecular alterations, functional information and enrichment pathway. [ABSTRACT FROM AUTHOR]

The article titled "G-Protein-Signaling Modulator 2 Expression and Role in a CD133+ Pancreatic Cancer Stem Cell Subset" has been retracted by the journal OncoTargets & Therapy. The retraction was prompted by concerns about the duplication of images from an unrelated article in Figure 5 of the published paper. The corresponding author provided an explanation that some experiments were conducted by a third party, but failed to provide satisfactory details or original data. The retracted article will remain online but will be marked as "Retracted." [Extracted from the article]

Aim: The principal goal of this meta-analysis is to test the hypothesis that circulating total adiponectin or certain fractions may represent a promising biological candidate in modulating the risk of colorectal cancer. Methods: The processes of paper identification, paper selection and data extraction were accomplished independently by two authors. Effect-size estimates were expressed as weighted mean difference (WMD) and 95% confidence interval (95% CI). A total of 31 papers including 48 qualified studies (7,554 patients with colorectal cancer and 9,798 controls) were meta-analyzed. Results: Pooling all studies found that circulating total adiponectin was significantly lower in patients with colorectal cancer than in controls (WMD: -0.76 μg/mL, 95% CI: -1.20 to -0.32, p=0.001), with significant heterogeneity (I2: 94.2%) and low publication bias (Egger’s p=0.336). By adiponectin fractions, the difference in high-molecular weight (HMW) adiponectin was com-parable between the two groups (WMD: -0.22 μg/mL, 95% CI: -0.70 to 0.25, p=0.350), while non-HMW adiponectin was significantly lower in patients with colorectal cancer than in controls (WMD: -0.27 μg/mL, 95% CI: -0.35 to -0.19, p,0.001), with marginal heterogeneity (I2: 52.3%). Subgroup analysis revealed that effect-size estimates were heterogeneous when grouping studies by cancer subtype, region, study design, matching status, gender and obesity. Further meta-regression analysis indicated that age and gender were significant potential sources of heterogeneity. The results showed the studied subgroups were not subject to publication bias (Egger’s p,0.1).Conclusion: Our data collectively indicate that low circulating total adiponectin, especially its non-HMW fraction, represents a promising risk factor for colorectal cancer. Further studies are needed to explore underlying mechanisms [ABSTRACT FROM AUTHOR]

Locally and regionally advanced renal cell carcinoma (RCC) can recur at high rates even after visually complete resection of primary disease. Both targeted therapies and immunotherapies represent potential agents that might help reduce recurrence of RCC in these patients. This paper reviews the current body of evidence defining their potential impact and examines the large Phase III randomized clinical trials that have been performed to assess the safety and efficacy of these systemic therapies in the adjuvant setting. Given that the findings from these trials have been predominantly negative, this paper also explores the role of other potential adjuvant agents, including single and combination agent targeted therapies and immunotherapies, whose use is currently limited to metastatic RCC. Finally, the use of radiation therapy and the use of advanced imaging modalities in RCC are also considered. [ABSTRACT FROM AUTHOR]

Pulmonary tuberculosis (TB) and lung cancer are both common diseases with poor prognosis and high mortality worldwide. The coexistence of the two diseases has rarely been reported while their relationship has been noted. Here we describe a patient diagnosed with both TB and squamous cell carcinoma in a single lesion. The patient had a cough for four months and polypnea for two months, with a smoking history of over 40 years. Chest computed tomography (CT) showed a lobular mass in the right hilar region, which was diagnosed as TB by transbronchial lung biopsy. The symptoms and CT findings indicated the possibility of lung cancer. So, the patient underwent a further lung biopsy at the periphery of the mass, which was confirmed as squamous cell carcinoma. This case illuminated that when the mass with cancer-like morphologic features and location instead of typical TB, even the initial pathological result shows TB, coexistence of the diseases should be considered. [ABSTRACT FROM AUTHOR]

Circular RNA PVT1 Promotes the Invasion and Epithelial-Mesenchymal Transition of Breast Cancer Cells through Serving as a Competing Endogenous RNA for miR-204-5p [Retraction] This retraction relates to this paper Bian Q. I Onco Targets Ther i . 2019;12:11817-11826. Concerns were raised regarding the alleged duplication of cell colony images in Figure 2C with the same images from other papers. [Extracted from the article]

background and relatively low resolution of photos captured for the wound healing assay. For Figure 3A on page 2691, all Transwell images were captured and saved in one folder labelled by experimental date. Two overlapping images from different visual fields were captured from one well but labelled incorrectly and inadvertently selected for Figure 3A. The correct Figures 2 and 3 are shown in Download Article. The authors apologize for these errors and advise they do not affect the results of the paper. Read the original article [ABSTRACT FROM AUTHOR]

This document is a corrigendum for an article titled "Synergism from the Combination of Ulinastatin and Curcumin Offers Greater Inhibition against Colorectal Cancer Liver Metastases via Modulating Matrix Metalloproteinase-9 and E-Cadherin Expression." The authors acknowledge an error in Figure 2C of the original article, where the images for cells treated with UTI and CUR were duplicated. However, they assure that this error does not affect the results of the paper. The corrigendum includes the correct Figure 2, which shows the effect of ulinastatin and curcumin on cell migration and invasion in colorectal cancer cells. [Extracted from the article]

Purpose: Anaplastic lymphoma kinase (ALK) inhibitors have transformed the management of non-small-cell lung cancer (NSCLC) patients with ALK gene rearrangement. This paper reports a new resistance mechanism to a second-generation ALK inhibitor, brigatinib. Case Report: A 43-year-old woman who had no history of smoking was diagnosed with stage IVa (T2bN2M1b) lung adenocarcinoma. After the first-line chemotherapy failed, the patient received crizotinib due to the presence of EML4-ALK fusion by next-generation sequencing (NGS). The patient had disease progression after 8 months on crizotinib, and a second NGS identified the ALK G1202R resistance mutation. Therefore, she was switched to brigatinib. After only 53 days of treatment with brigatinib, the patient developed a new 1.6× 1.2 cm lesion in the mediastinal lymph node. A third NGS testing revealed a new form of NTRK rearrangement (LIPI-NTRK1). The patient died 16 months after diagnosis. Conclusion: This paper provides new insights into the primary resistance to brigatinib in NSCLC patients carrying ALK G1202R mutation. The new fusion form of NTRK rearrangement was detected, which may provide potential treatment options after brigatinib resistance. [ABSTRACT FROM AUTHOR]

This retraction relates to this paper Wang Y, Liu Y, Du X, Ma H, Yao J. I Onco Targets Ther i . 2020;13:1909-1919. Specifically, The western blot image for Figure 2B, MCF7/ADR, MDR1 appears to have been duplicated with the image for Figure 4C, MCF7/ADR, p62, which has been flipped. [Extracted from the article]

As verifying the validity of the published work is core to the integrity of the scholarly record, we are therefore retracting the article and the authors were notified of this. This retraction relates to this paper Li W, Li X, Li X, et al. I Onco Targets Ther i . 2020;13:3129-3139. [Extracted from the article]

This retraction relates to this paper Nan P, Niu Y, Wang X, Li Q. I Onco Targets Ther i . 2019;12:6917-6925. As verifying the validity of the published work is core to the integrity of the scholarly record, we are therefore retracting the article and the authors were notified of this. [Extracted from the article]

This retraction relates to this paper Zhao X, Zhang W, Ji W. I Onco Targets Ther i . 2018;11:3619-3635. As the findings could not be verified the Editor and Publisher made the decision to retract the article and the authors were notified of this. [Extracted from the article]

This retraction relates to this paper Wu J, Du M, Zhang Q, et al. I Onco Targets Ther i . 2018;11:7483-7492. Specifically, The images for Figure 2E, CNE-2, Migration, si-UCA1 and Invasion, siRNA-NC, have been duplicated with the images for Figure 4C, CNE-2, Migration, Inhibitor NC+si-UCA1 and Inhibitor NC+siRNA-NC, respectively. [Extracted from the article]

Since publication, concerns have been raised about the integrity of the data in the article. This retraction relates to this paper Jiang SB, He XJ, Xia YJ, et al. I Onco Targets Ther i . 2016;9:2305-2315. [Extracted from the article]

Specifically, The image for Figure 5C, NC, has overlap with the image for Figure 6D, NC. This retraction relates to this paper Sun F, Wu K, Yao Z, et al. I Onco Targets Ther i . 2020;13:6755-6765. [Extracted from the article]

As verifying the validity of the published work is core to the integrity of the scholarly record, we are therefore retracting the article and the authors were notified of this. This retraction relates to this paper Wang C, Li X, Zhang J, Ge Z, Chen H, Hu J. I Onco Targets Ther i . 2018;11:7853-7864. [Extracted from the article]

As verifying the validity of the published work is core to the integrity of the scholarly record, we are therefore retracting the article and the authors were notified of this. This retraction relates to this paper Chen H, Liu T, Ouyang H, et al. I Onco Targets Ther i . 2020;13:7125-7136. [Extracted from the article]

This retraction relates to this paper Lin Y, Huang G, Jin H, Jian Z. I Onco Targets Ther i . 2020;13:4509-4521. As verifying the validity of the published work is core to the integrity of the scholarly record, we are therefore retracting the article and the authors were notified of this. [Extracted from the article]

This retraction relates to this paper Qu C, Dai C, Guo Y, Qin R, Liu J. I Onco Targets Ther i . 2019;12:101-111. As verifying the validity of the published work is core to the integrity of the scholarly record, we are therefore retracting the article and the authors were notified of this. [Extracted from the article]

This retraction relates to this paper Xing Y, Zhang J, Xu H. I Onco Targets Ther i . 2016;9:3939-3949. Specifically, Images from Figure 3C, Migration, Treg-C+S and Migration, GIST882-sorafenib have been duplicated. [Extracted from the article]

We, the Editor and Publisher of I OncoTargets and Therapy i are retracting the published article. This retraction relates to this paper Peng T, Li Z, Li D, Wang S. I Onco Targets Ther i . 2019;12:1893-1903. [Extracted from the article]

We have been informed in our decision-making by our policy on publishing ethics and integrity and the COPE guidelines on retractions. This retraction relates to this paper Cheng N, Guo Y. I Onco Targets Ther i . 2017;10:5843-5853. [Extracted from the article]

This retraction relates to this paper Liu D, Zhao J, Wang H, Li H, Li Y, Qin W. I Onco Targets Ther i . 2020;13:11975-11990. We have been informed in our decision-making by our policy on publishing ethics and integrity and the COPE guidelines on retractions. [Extracted from the article]

This retraction relates to this paper Zhou K, Li S, Du G, et al. I Onco Targets Ther i . 2019;12:7095-7109. As verifying the validity of the published work is core to the integrity of the scholarly record, we are therefore retracting the article and the authors were notified of this. [Extracted from the article]

Since publication, concerns have been raised about the duplication of images in this article with those from other unrelated articles. This retraction relates to this paper Jia Z, Li W, Bian P, Liu H, Pan D, Dou Z. I Onco Targets Ther i . 2020;13:9365-9376. [Extracted from the article]

At the authors request, we the Editor and Publisher of I OncoTargets and Therapy i are retracting the published article. This retraction relates to this paper Wang J, Gao J, Chen Q, et al. I Onco Targets Ther i . 2020;13:9333-9347. [Extracted from the article]

We have been informed in our decision-making by our policy on publishing ethics and integrity and the COPE guidelines on retractions. This retraction relates to this paper Chen L, Liu J, Tang T, et al. I Onco Targets Ther i . 2018;11:7955-7965. [Extracted from the article]

Since publication, concerns have been raised about the integrity of the data in the article and it was found some of the images had been duplicated. This retraction relates to this paper Yu J, Sun S, Mao W, Xu B, Chen M. I Onco Targets Ther i . 2021;14:3833-3848. [Extracted from the article]

This retraction relates to this paper Hong F, Li Y, Ni H, Li J. I Onco Targets Ther i . 2018;11:3485-3494. We, the Editor and Publisher of I OncoTargets and Therapy i are retracting the published article. [Extracted from the article]

This retraction relates to this paper Xia C, Jiang H, Ye F, Zhuang Z. I Onco Targets Ther i . 2019;12:8319-8328. Since publication, concerns have been raised about the integrity of the data in the article. We, the Editor and Publisher of I OncoTargets and Therapy i are retracting the published article. [Extracted from the article]

We, the Editor and Publisher of I OncoTargets and Therapy i are retracting the published article. This retraction relates to this paper Wu G, Ma Z, Qian J, Liu B. I Onco Targets Ther i . 2015;8:2067-2074. [Extracted from the article]

This retraction relates to this paper Wang M, Wu Q, Fang M, Huang W, Zhu H. I Onco Targets Ther i . 2019;12:9513-9525. We, the Editor and Publisher of I Onco Targets and Therapy i are retracting the published article. Since publication, concerns have been raised about the integrity of the data in the article. [Extracted from the article]

This retraction relates to this paper Xie R, Zhang Y, Shen C, Cao X, Gu S, Che X. I Onco Targets Ther i . 2015;8:1119-1127. Since publication, concerns have been raised about the integrity of the data in the article. [Extracted from the article]

The Editor and Publisher of I OncoTargets and Therapy i are retracting the published article. This retraction relates to this paper Zhou S, Cui Y, Yu D, Liang J, Zhang M, Ye W. I Onco Targets Ther i . 2017;10:2527-2538. [Extracted from the article]

This retraction relates to this paper Zhang Q, Xu L, Wang J, et al. I Onco Targets Ther i . 2021;14:1187-1204. At the authors request, the Editor and Publisher of I OncoTargets and Therapy i are retracting the published article. [Extracted from the article]

This document is a retraction notice for an article titled "miR-182 Promotes Tumor Growth and Increases Chemoresistance of Human Anaplastic Thyroid Cancer by Targeting Tripartite Motif 8." The retraction is due to concerns about the duplication of images from other unrelated articles in Figures 2 and 3 of the paper. The authors did not respond to queries or provide an explanation for the duplicated images. The article will remain online but will be digitally watermarked as "Retracted." [Extracted from the article]

Tenosynovial giant cell tumor (TGCT) is a neoplasm of the joint synovium that can have severe impacts on joint mobility, function, and quality of life. Traditionally, treatment modalities included partial or complete surgical synovectomy, radiotherapy (typically as an adjunct to surgery), and watchful monitoring (no medical or surgical intervention). However, these approaches have been met with varying degrees of success and high recurrence rates, as well as onerous complications and clinical sequelae. Pexidartinib, a colony-stimulating factor 1 receptor (CSF1R) inhibitor, presents a promising molecular approach that targets a neoplastic driver of TGCT. While the introduction of pexidartinib allows clinicians to avoid the significant morbidity associated with traditional treatment options, there are also defined risks associated with pexidartinib treatment. Therefore, patient selection is critical in optimizing treatment modalities in TGCT. The purpose of this literature review is to identify the TGCT patient population that would derive maximal benefit with minimal risk from pexidartinib, and to determine the specific indications and contraindications for selecting pexidartinib over other therapeutic approaches. Specifically, this paper compares the efficacy and safety profile of pexidartinib across clinical and preclinical studies to that of surgery, radiotherapy, and watchful monitoring. Rates of improvement in joint mobility, pain, and recurrence-free survival across studies of pexidartinib have been encouraging. The most common adverse events are mild (hypopigmentation of the hair) or reversible (transient aminotransferase elevation). Severe or permanent adverse events (notably cholestatic hepatotoxicity) are rare. While the optimal treatment strategy remains highly dependent on a patient's clinical circumstances and treatment goals, pexidartinib has surfaced as a promising therapeutic in cases where the morbidity of surgery or radiotherapy outweighs the benefits. [ABSTRACT FROM AUTHOR]

At the authors request, the Editor and Publisher of I OncoTargets and Therapy i wish to retract the published article. This retraction relates to this paper Ding X, Du J, Mao K, Wang X, Ding Y, Wang F. I Onco Targets Ther i . 2019;12:3255-3265. [Extracted from the article]

I Onco Targets Ther i . 2020;13:8907-8917 At the authors request, the Editor and Publisher of I OncoTargets and Therapy i are retracting the published article. This retraction relates to this paper Song X, Xu X, Ren X, Ruan X, Wang Y, Yao TT. [Extracted from the article]

This retraction relates to this paper Sun H, Zhang Z, Zhang T, et al. I Onco Targets Ther i . 2019;12:10227-10237 The Editor and Publisher of I OncoTargets and Therapy i are retracting the published article. An investigation found, specifically, The image for Figure 1D, CSE(%) 0, has been duplicated with the same image for Figure 3C, CSE(%) 0; Stattic(µM) 0.5. Resveratrol Reverses Cigarette Smoke-Induced Urocystic Epithelial-Mesenchymal Transition via Suppression of STAT3 Phosphorylation in SV-HUC-1-Immortalized Human Urothelial Cells [Retraction]. [Extracted from the article]

The Editor and Publisher of I OncoTargets and Therapy i are retracting the published article. This retraction relates to this paper Tan T, Chen J, Hu Y, et al. I Onco Targets Ther i . 2019;12:5111-5122. [Extracted from the article]

Specifically, Figure 2Ba, HL60 cells, PCA (1 µM), appears to have been duplicated with the same image for Figure 3Ba, U937 cells, PCA (1 µM), and Figure 3Ba, U937 cells, PCA (2 µM), which has been flipped. This retraction relates to this paper Ye QD, Liao XL, Fu P, Dou JY, Chen K, Jiang H. I Onco Targets Ther i . 2016;9:6953-6963. [Extracted from the article]

This retraction relates to this paper Yang J, He D, Peng Y, et al. I OncoTargets and Therapy i . 2017;10:5209-5217. Figure 2A, A549, Migration, (0mg/mL), appears to have been duplicated with the same images for Figure 2A, A549, Migration, (0.5mg/mL); Invasion (0mg/mL); Invasion, (0.5mg/mL) and Figure 2B, H1299, Invasion, (0mg/mL). [Extracted from the article]

Introduction: The results of the earlier published studies on the association between KIF1B (rs17401966) polymorphism and hepatocellular carcinoma (HCC) risk are inconclusive. Hence, we performed this meta-analysis to evaluate the relationship between KIF1B (rs17401966) polymorphism and HCC risk. Methods: Databases including PubMed, Web of Science and the Cochrane Library and bibliographies of relevant papers were screened to identify relevant studies published up to March 25, 2018. Pooled ORs and 95% CIs were calculated to evaluate the association. The subgroup analysis was conducted based on ethnicity, age, region and environment. A total of 19 studies from 11 eligible articles published from 2010 to 2016, with 8,741 cases and 10,812 controls, were included. Results: The pooled results indicated that the association between KIF1B (rs17401966) polymorphism and the decreased HCC risk was significant. Subgroup analysis stratified by ethnicity showed the same association in Chinese, but not in non-Chinese population. When stratified by age, both old and young patients showed a decrease in HCC risk. When stratified by region, we detected the same association in Chinese in southern China. Similarly when stratified by environment, we observed the same association in Chinese in inland areas; however, no statistically significant association was observed in those in coastal areas. Conclusion: This meta-analysis suggested that KIF1B (rs17401966) polymorphism could decrease HCC risk in Chinese and in overall population, but not in non-Chinese. This association remained significant in Chinese in southern China and inland areas, but not in those in northern and central China and coastal areas. Further large-scale multicenter studies are warranted to confirm these findings. [ABSTRACT FROM AUTHOR]

Background and aims: Several studies were conducted to explore the prognostic value of platelet-to-lymphocyte ratio (PLR) in pancreatic cancer and have reported contradictory results. This study aims to summarize the prognostic role of PLR in pancreatic cancer. Materials and methods: Embase, PubMed and Cochrane Library were completely searched. The cohort studies focusing on the prognostic role of PLR in pancreatic cancer were eligible. The overall survival (OS) and progression-free survival (PFS) were analyzed. Results: Fifteen papers containing 17 cohort studies with pancreatic cancer were identified. The results showed patients that with low PLR might have longer OS when compared to the patients with high PLR (hazard ratio=1.28, 95% CI=1.17-1.40, P＜0.00001; I2=42%). Similar results were observed in the subgroup analyses of OS, which was based on the analysis model, ethnicity, sample size and cut-off value. Further analyses based on the adjusted potential confounders were conducted, including CA199, neutrophil-to-lymphocyte ratio, modified Glasgow Prognostic Score, albumin, C-reactive protein, Eastern Cooperative Oncology Group, stage, tumor size, nodal involvement, tumor differentiation, margin status, age and gender, which confirmed that low PLR was a protective factor in pancreatic cancer. In addition, low PLR was significantly associated with longer PFS when compared to high PLR in pancreatic cancer (hazard ratio=1.27, 95% CI=1.03-1.57, P=0.03; I2=33%). Conclusion: In conclusion, it was found that high PLR is an unfavorable predictor of OS and PFS in patients with pancreatic cancer, and PLR is a promising prognostic biomarker for pancreatic cancer. [ABSTRACT FROM AUTHOR]

Purpose: miRNAs can act as oncogenes or tumor suppressors and participate in the development and progression of tumors, thus affecting the prognosis and survival of cancer patients. In this paper, we mainly studied the role of miR-1826 in prostate cancer. Patients and Methods: The expression of miR-1826 was studied by quantitative real-time PCR (qRT-PCR). Kaplan–Meier curves were used to analyze the relationship between the expression of miR-1826 and the survival rate of PC patients. Cox regression analysis was used to study the risk factors affecting the prognosis of PC patients. PC cells were transfected with miR-1826 mimic, mimic negative control (mimic NC), miR-1826 inhibitor, or inhibitor NC. The effect of miR-1826 on the proliferation of PC cells was studied by the CCK-8 method and colony formation assay. Transwell assays were used to detect the effect of miR-1826 on the migratory and invasive abilities of tumor cells. Results: The expression of miR-1826 in PC tissues was lower than that in adjacent normal tissues, and that the expression levels of miR-1826 in four PC cell lines were all lower than normal human prostate epithelial cell lines. Patients with low expression of miR-1826 had shorter overall survival compared with those with high expression. The downregulation of miR-1826 promoted PC cell proliferation, migration, and invasion. Conclusion: In summary, the low expression of miR-1826 may promote the progression of PC, and the low expression of miR-1826 is also associated with a poor prognosis in PC patients. [ABSTRACT FROM AUTHOR]