Differential expression of Axl and correlation with invasion and multidrug resistance in cancer cells
Authors: Lili Jiang
Xiance Sun
Yongfu Zhao
Fengjuan Yang
Li Jia
Zhaohai Zhang
Journal: Cancer Investigation (2012)
Discipline: CLINICAL MEDICINE
Keywords: Axl receptor tyrosine kinases; drug-resistant cancer cells; RNAi; invasion; proliferation
Affiliations: College of Laboratory Medicine, Dalian Medical University, Dalian, China., Department of Occupational and Environmental Health, School of Public Health, Dalian Medical University,
Dalian, China,3, Department of Foreign Language, Dalian Medical University,
Dalian, China,4, Haining Senior High School,
Haining City, China5, College of Laboratory Medicine, Dalian Medical University,
Dalian, China,1

Abstract:  Dysregulation of Axl receptor tyrosine kinases is implicated in the pathogenesis of several sensitive and refractory cancers. In this study we showed that Axl expression was upregulated in drug-resistant cancer cells, as compared to those in parental cells. Downregulation of Axl expression by RNAi led to a decrease of K562/ADR and MCF-7/ADR cells invasion, proliferation in soft agar, and increased cells chemosensitivity in vitro. In nude mice bearing xenografts, downregulation of Axl in MDR cells enhanced the anticancer activity of intraperitoneally applied chemotherapeutic drugs. Our observations suggest that Axl represents a promising gene for overcoming MDR in cancer therapy. 

Retracted: No

PubPeer comments:
  Figure 2. Downregulation of Axl impedes K562 ADR and MCF-7 ADR cells anchorage-independent growth in vitro. (A, B) The K562 ADR and MCF-7 ADR cells were transfected with Axl siRNA and control siRNA. The Axl, protein levels were analyzed by Western blot analysis, respectively. Relative signal intensities of Axl, levels were normalized against those of GAPDH  GAPDH band somehow reminds me of the loading control in Fig 2E from Jia et al (2007), [ siRNA targeted against matrix metalloproteinase 11 inhibits the metastatic capability of murine hepatocarcinoma cell Hca-F to lymph nodes ] . ![file] , 
 Concern about Figures 1 and 2. Two lanes in Figure 1A look very similar to lanes in Figure 2B, when one of the 2 figures is rotated 180 degrees. Illustrated here with red and blue boxes. ![file] , 
 #1 In another thread, Bacillus Mannanilyticus noted the later activities of the GAPDH panel from Fig 1A. https: pubpeer.com publications B898A0401F614CA6DB568619BFB1D0#3 ![] The first lane of that slice is unexpectedly similar to the first lane of a **third** loading control, in Fig 5A of  Functional roles of glycogene and N-glycan in multidrug resistance of human breast cancer cells [(Ma et al 2013)] . ![] Update: Another appearance of the same loading control in Fig 5A of  Glycogenes mediate the invasive properties and chemosensitivity of human hepatocarcinoma cells [(Guo et al 2013)] . ![file] , 
 Correction, [19 April 2021] . ---------------------------------------- When this article was first published online, information in Figure 1 and Figure 2 are incorrect. Specifically, Figure 1A (blot of Axl) overlapped Figure 2A (blot of Axl), caused by the checking failure. Similarly, Figure 1A and Figure 2A (blot of the GAPDH) was wrong used because of the huge number of data. The corrected version of Figure 1 and Figure 2 are as follows: ![] ![] --------------------------------------------- Background [here] . ,